Academic literature on the topic 'Pulmonary acute inflammation'
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Journal articles on the topic "Pulmonary acute inflammation"
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Arndt, Patrick G., Brian Strahan, Yue Wang, Chunmei Long, Keisuke Horiuchi, and Bruce Walcheck. "Leukocyte ADAM17 Regulates Acute Pulmonary Inflammation." PLoS ONE 6, no. 5 (May 16, 2011): e19938. http://dx.doi.org/10.1371/journal.pone.0019938.
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Savin, Innokenty A., Marina A. Zenkova, and Aleksandra V. Sen’kova. "Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches." International Journal of Molecular Sciences 23, no. 23 (November 29, 2022): 14959. http://dx.doi.org/10.3390/ijms232314959.
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Pulmonary fibrosis is a chronic progressive lung disease that steadily leads to lung architecture disruption and respiratory failure. The development of pulmonary fibrosis is mostly the result of previous acute lung inflammation, caused by a wide variety of etiological factors, not resolved over time and causing the deposition of fibrotic tissue in the lungs. Despite a long history of study and good coverage of the problem in the scientific literature, the effective therapeutic approaches for pulmonary fibrosis treatment are currently lacking. Thus, the study of the molecular mechanisms underlying the transition from acute lung inflammation to pulmonary fibrosis, and the search for new molecular markers and promising therapeutic targets to prevent pulmonary fibrosis development, remain highly relevant tasks. This review focuses on the etiology, pathogenesis, morphological characteristics and outcomes of acute lung inflammation as a precursor of pulmonary fibrosis; the pathomorphological changes in the lungs during fibrosis development; the known molecular mechanisms and key players of the signaling pathways mediating acute lung inflammation and pulmonary fibrosis, as well as the characteristics of the most common in vivo models of these processes. Moreover, the prognostic markers of acute lung injury severity and pulmonary fibrosis development as well as approved and potential therapeutic approaches suppressing the transition from acute lung inflammation to fibrosis are discussed.
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Eckle, Tobias, Michael Koeppen, and Holger K. Eltzschig. "Role of Extracellular Adenosine in Acute Lung Injury." Physiology 24, no. 5 (October 2009): 298–306. http://dx.doi.org/10.1152/physiol.00022.2009.
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Acute lung injury (ALI) is a lung disease characterized by pulmonary edema and severe hypoxia. The past decade hosted a search for endogenous mechanisms controlling lung inflammation and pulmonary edema during ALI. As such, recent evidence indicates extracellular adenosine in orchestrating the resolution of pulmonary edema and inflammation during ALI.
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Spond, J., N. Case, R. W. Chapman, Y. Crawley, R. W. Egan, J. Fine, J. A. Hey, et al. "Inhibition of experimental acute pulmonary inflammation by pirfenidone." Pulmonary Pharmacology & Therapeutics 16, no. 4 (August 2003): 207–14. http://dx.doi.org/10.1016/s1094-5539(03)00026-9.
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Singh, Baljit, Jacqueline W. Pearce, Lakshman N. Gamage, Kyathanahalli Janardhan, and Sarah Caldwell. "Depletion of pulmonary intravascular macrophages inhibits acute lung inflammation." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 2 (February 2004): L363—L372. http://dx.doi.org/10.1152/ajplung.00003.2003.
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Pulmonary intravascular macrophages (PIMs) are present in ruminants and horses. These species are highly sensitive to acute lung inflammation compared with non-PIM-containing species such as rats and humans. There is evidence that rats and humans may also recruit PIMs under certain conditions. We investigated precise contributions of PIMs to acute lung inflammation in a calf model. First, PIMs were recognized with a combination of in vivo phagocytic tracer Monastral blue and postembedding immunohistology with anti-CD68 monoclonal antibody. Second, gadolinium chloride depleted PIMs within 48 h of treatment ( P < 0.05). Finally, PIMs contain TNF-α, and their depletion reduces cells positive for IL-8 ( P < 0.05) and TNF-α ( P < 0.05) and histopathological signs of acute lung inflammation in calves infected with Mannheimia hemolytica. The majority of IL-8-positive inflammatory cells in lung septa of infected calves were platelets. Platelets from normal cattle contained preformed IL-8 that was released upon in vitro exposure to thrombin ( P < 0.05). These novel data show that PIMs, as the source of TNF-α, promote recruitment of inflammatory cells including IL-8-containing platelets to stimulate acute inflammation and pathology in lungs. These data may also be relevant to humans due to our ability to recruit PIMs.
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Selby, C., and W. Macnee. "Factors Affecting Neutrophil Transit During Acute Pulmonary Inflammation: Minireview." Experimental Lung Research 19, no. 4 (January 1993): 407–28. http://dx.doi.org/10.3109/01902149309064355.
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Mirakaj, Valbona, Cyril A. Thix, Stefanie Laucher, Carina Mielke, Julio C. Morote-Garcia, Marthe A. Schmit, Janek Henes, Klaus E. Unertl, David Köhler, and Peter Rosenberger. "Netrin-1 Dampens Pulmonary Inflammation during Acute Lung Injury." American Journal of Respiratory and Critical Care Medicine 181, no. 8 (April 15, 2010): 815–24. http://dx.doi.org/10.1164/rccm.200905-0717oc.
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Mancuso, Peter. "Obesity and lung inflammation." Journal of Applied Physiology 108, no. 3 (March 2010): 722–28. http://dx.doi.org/10.1152/japplphysiol.00781.2009.
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The prevalence of obesity has increased dramatically worldwide, predisposing individuals to an increased risk of morbidity and mortality due to cardiovascular disease and type 2 diabetes. Less recognized is the fact that obesity may play a significant role in the pathogenesis of pulmonary diseases through mechanisms that may involve proinflammatory mediators produced in adipose tissue that contribute to a low-grade state of systemic inflammation. In animal models, inflammatory responses in the lung have been shown to influence the production of the adipocytokines, leptin and adiponectin, cytokines, acute phase proteins, and other mediators produced by adipose tissue that may participate in immune responses of the lung. An increased adipose tissue mass may also influence susceptibility to pulmonary infections, enhance pulmonary inflammation associated with environmental exposures, and exacerbate airway obstruction in preexisting lung disease. An increased understanding of the mechanisms by which obesity influences pulmonary inflammation may facilitate the development of novel therapeutic interventions for the treatment of lung disease.
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Jung, Ayoung, Sung-Hyun Kim, Jun-Young Yang, Jayoung Jeong, Jong Kwon Lee, Jae-Ho Oh, and Jin Hee Lee. "Effect of Pulmonary Inflammation by Surface Functionalization of Zinc Oxide Nanoparticles." Toxics 9, no. 12 (December 6, 2021): 336. http://dx.doi.org/10.3390/toxics9120336.
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Zinc oxide nanoparticles (ZnO NPs) are used in various industries such as food additives, cosmetics, and biomedical applications. In this study, we evaluated lung damage over time by three types of ZnO NPs (L-serine, citrate, and pristine) following the regulation of functional groups after a single intratracheal instillation to rats. The three types of ZnO NPs showed an acute inflammatory reaction with increased LDH and inflammatory cell infiltration in the alveoli 24 h after administration. Especially in treatment with L-serine, citrate ZnO NPs showed higher acute granulocytic inflammation and total protein induction than the pristine ZnO NPs at 24 h. The acute inflammatory reaction of the lungs recovered on day 30 with bronchoalveolar fibrosis. The concentrations of IL-4, 6, TNF-α, and eotaxin in the bronchoalveolar lavage fluid (BALF) decreased over time, and the levels of these inflammation indicators are consistent with the following inflammatory cell data and acute lung inflammation by ZnO NP. This study suggests that single inhalation exposure to functionalized ZnO NPs may cause acute lung injury with granulocytic inflammation. Although it can recover 30 days after exposure, acute pulmonary inflammation in surface functionalization means that additional studies of exposure limits are needed to protect the workers that produce it.
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Ziablitsev, D. S., O. O. Dyadyk, and S. V. Ziablitsev. "ACTIVITY OF ANGIOTENSIN-CONVERSING ENZYME-2 IN ACUTE PULMONARY INFLAMMATION." Medical Science of Ukraine (MSU) 17, no. 3 (September 30, 2021): 3–14. http://dx.doi.org/10.32345/2664-4738.3.2021.01.
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Relevance. Angiotensin converting enzyme-2 (ACE2), which is the gateway to coronavirus, is also an important component of the tissue renin-angiotensin system with a number of anti-inflammatory effects. It is known that ACE2 is expressed in the lungs of patients with coronavirus pneumonia, but it is not clear how this depends on the stages of development and the severity of inflammation.
Objective: to establish the effect of acute inflammation on pulmonary expression of angiotensin-converting enzyme-2.
Material and methods. In Wistar rats (n=20), in compliance with bioethical standards, a sterile nylon thread 2.5 cm long and 0.2 mm thick to a depth of 2.5 cm was introduced into the trachea. The animals were observed and removed from the experiment at 7, 14, 21 and 28 days, microscopic and immunohistochemical (monoclonal antibodies against ACE2; clone 4G5.1; EMD Millipore Corporation; Temecula, CA US) studies were performed.
Results. The microscopic picture of the lungs indicated the development of acute bronchopulmonary inflammation during the first week, the formation of peribronchial and alveolar abscesses in the second week with the onset of resolution of bronchopneumonia with the organization of abscesses in the third week and the development of diffuse fibrosis of the parenchyma and vascular hyalinosis in the fourth week of observation. The exudative phase of acute inflammation was accompanied by inhibition of ACE2 activity in bronchial epithelial cells, type II alveolocytes and vascular endothelium. With the transition of inflammation to the stage of proliferation and fibrosis, ACE2 activity was restored.
Conclusion. The detected phase change in ACE2 activity can cause a wavy recurrent course of coronavirus infection, since an increase in the amount of ACE2 protein during attenuation of acute inflammation contributes to an increase in target cell infection.
Dissertations / Theses on the topic "Pulmonary acute inflammation"
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Simpson, A. John. "The effects of elafin gene augmentation on acute pulmonary inflammation." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/25189.
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The hypothesis driving this work was that genetic augmentation of elafin may protect the lung against acute inflammatory injury. A replication-deficient adenovirus encoding human elafin cDNA under the control of the powerful murine cytomegalovirus promoter (Ad-elafin) was used to augment elafin production because of the natural tropism of adenovirus for respiratory epithelium. Ad-elafin significantly protected pulmonary epithelial cells against the effects of both HNE and whole activated human neutrophils in vitro. These findings were extended by studying the effect of Ad-elafin on pulmonary neutrophilia induced by lipopolysaccharide (LPS) in mice. Intratracheal (IT) Ad-elafin, administered in doses low enough to obviate overt vector-induced inflammation, significantly augmented LPS-mediated neutrophilia. In addition, LPS significantly up-regulated elafin secretion in Ad-elafin transfected murine airways and in Ad-elafin transfected human pulmonary epithelial cells. The demonstration of a cytoprotective effect for a low molecular weight, cationic elastase inhibitor capable of augmenting neutrophil recruitment during inflammation suggested a potential antimicrobial function for elafin. Elafin was shown to have significant antimicrobial activity against the respiratory pathogens Pseudomonas aeruginosa and Staphylococcus aureus. On the basis of these observations, the hypothesis that elafin may be protective against inflammatory injury was tested in vivo. Low dose IT Ad-elafin (3x107 plaque forming units) was associated with a significant reduction in acute lung injury induced by Pseudomonas aeruginosa in mice. These findings suggest that genetic augmentation of endogenous host defence molecules can protect the lung against acute inflammatory injury. They further suggest that adenoviral constructs containing selective promoters may allow inflammation-specific expression of transgene using low doses of vector.
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Kurti, Stephanie P. "The impact of lifestyle, age, and sex on systemic and airway inflammation and oxidative stress." Diss., Kansas State University, 2017. http://hdl.handle.net/2097/35294.
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Doctor of PhilosophyDepartment of Kinesiology
Craig A. Harms
The overall aim of this dissertation was to determine the impact of lifestyle (i.e. habitual and acute physical activity and diet), age, and sex on systemic and airway inflammation and oxidative stress. In study 1 (Chapter 2) we examined the impact of habitual physical activity level on the post-prandial airway inflammatory response following an acute bout of moderate intensity exercise. Results indicated that the mean exhaled nitric oxide (eNO; marker of airway inflammation) response increased for all groups at two hours post high-fat meal (HFM) (~6%) and returned to baseline by four hours post-HFM. However, there was a varying eNO response from baseline to four hours in the group that exercised in the post-prandial period compared to the group that remained sedentary. These findings suggest airway inflammation occurs after a HFM when exercise is performed in the post-prandial period, regardless of habitual physical activity level. In study 2 (Chapter 3) we investigated the post-prandial oxidative stress response to meals of varying calories and fat. Specifically, we assessed the post-prandial airway and systemic 8-isoprostane (a marker of oxidative stress) responses to meals with moderate-fat (8.5 kcal/kg of bodyweight) and high-fat content (17 kcal/kg of bodyweight) from baseline to six hours post-meal in a randomized crossover design. This study revealed that systemic 8-isoprostane increased from baseline to six hours post-meal (38.3%), but there was no difference between the moderate-fat meal (MFM) and HFM conditions. There were no changes in airway 8-isoprostane from baseline to six hours post-MFM or HFM, or between the MFM and HFM conditions. Lastly, in study 3 (Chapter 4), we were interested in examining 8-isoprostane responses in older adults, since 8-isoprostane has been reported to increase with age. Previous research also suggests that older women (OW) and older men (OM) have differences with regard to prevalence and severity of late-onset asthma. In this study, we sought to determine whether the airway 8-isoprostane response to a strenuous bout of exercise was different in OW compared to OM. A secondary aim was to determine whether post-exercise 8-isoprostane generation was correlated with decrements in lung function. Our results showed that the generation of 8-isoprostane from pre- to post-exercise increased ~74±77% in OW and decreased ~12±50% in OM. The decrease in 8-isoprostane generation was not correlated with improvements in lung function from pre- to post-exercise. These findings collectively contribute to the literature by enhancing our understanding of the impact of lifestyle factors, age and sex on modifying and potentially mitigating the risk of developing chronic diseases.
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Miettinen, J. (Johanna). "Studies on bone marrow-derived stem cells in patients with acute myocardial infarction." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514293924.
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Abstract Intracoronary administration of autologous bone marrow derived stem cells (BMC) has been postulated to repair the myocardial damage in patients who have suffered acute ST-elevation myocardial infarction (STEMI). The aim of this study was to find determinants for the left ventricular functional recovery after BMC treatment of STEMI and to study the effect of BMC treatment on different biochemical and clinical parameters associated with the outcome of STEMI patients. In this study, STEMI patients treated with thrombolysis were randomly assigned to receive either intracoronary BMC (n=39) or placebo (n=39) into the infarct related artery at the time of percutaneous coronary intervention. The efficacy of the BMC treatment was assessed by measurement of the change of left ventricular ejection fraction (LVEF) from baseline to six months after STEMI. Two-dimensional echocardiography was used to assess PA pressure, LV systolic and diastolic function. Blood samples were drawn for biochemical determinations at several time points and BMCs were cultured in the laboratory for in vitro analyses. In the BMC group, the most powerful determinant of the change of LVEF was the baseline LVEF. Patients with baseline LVEF at or below the median (≤62.5%) experienced a more marked improvement of LVEF than those above the median. Elevated levels of N-terminal probrain natriuretic peptide (NT-proBNP) and N-terminal proatrial natriuretic peptide (NT-proANP) were also associated with an improvement of LVEF in the BMC group. However, no difference was observed between the BMC group and the placebo group in the changes of the levels of NT-proANP, NT-proBNP or any of the inflammatory markers measured. The BMC group showed a trend toward a reduction of peak PA pressure, while the placebo group had a significant increase of peak PA pressure at 6 months. In addition, there was a greater improvement in the LV diastolic function, assessed in quartiles, in the BMC group. The in vitro studies of BMCs revealed that exposure to tumor necrosis factor alpha (TNF-α) significantly enhanced the proliferation of BMCs and resulted in activation of immunosuppression by altering the expression of several immunosuppressive proteins. In conclusion, low baseline LVEF as well as high levels of natriuretic peptides NT-proANP and NT-proBNP, which reflect the severity of the hemodynamic and neurohumoral reactions evoked by the myocardial damage, have a considerable association to a better response to stem cell therapy after an acute STEMI. BMC therapy also prevents the increase of PA pressure and improves the cardiac diastolic function. Based on in vitro studies, the inflammatory cytokine TNF-α seems to evoke an enhanced proliferation of the bone marrow-derived mesenchymal stem cells and activation of several immunosuppressive defence mechanismsTiivistelmä Sydäninfarktipotilaiden sepelvaltimoon pallolaajennuksen yhteydessä injektoitujen kantasolujen tiedetään parantavan hieman sydämen pumppauskykyä, mutta taustalla olevaa mekanismia ei tunneta. Kantasoluhoidon onnistumiseen vaikuttavia tekijöitä on tutkittu vasta vähän, eikä myöskään sitä tiedetä, miksi kaikki potilaat eivät hyödy kantasoluhoidosta. Tämän tutkimuksen tavoitteena oli selvittää infarktialueelle annetun kantasoluhoidon vaikutuksia äkillisen ST-nousuinfarktin (STEMI) sairastaneissa potilaissa, ja etsiä hoidon onnistumiseen vaikuttavia tekijöitä. Tutkimuksessa käytettiin potilasaineistoa, johon otettiin 78 äkilliseen sydäninfarktiin sairastunutta potilasta, jotka hoidettiin liuotushoidolla ja sen jälkeen pallolaajennuksella. Puolet potilaista satunnaistettiin saamaan lumeliuosta ja puolet omaa luuydinsolukkoaan (BMC), joka ruiskutettiin pallolaajennuksen yhteydessä sepelvaltimon kautta infarktialueelle. Hoidon vaikusta tutkittiin mittaamalla angiografian avulla vasemman kammion ejektiofraktion (LVEF) muutosta lähtötilanteen ja kuuden kuukauden seurannan välillä. Lisäksi sydämen ultraäänitutkimuksella määritettiin keuhkovaltimopainetta ja vasemman kammion systolista ja diastolista toimintaa. Potilaista otettiin lisäksi verinäytteitä, joista määritettiin erilaisia tulehdusmerkkiaineita ja natriureettisia peptidejä. Lisäksi potilaista kerättyjä luuydinkantasoluja viljeltiin laboratoriossa in vitro-analyyseja varten. Tutkimuksessa todettiin, että LVEF ennen kantasoluhoitoa oli voimakkain ennustetekijä suotuisalle LVEF:n muutokselle kantasoluhoidon jälkeen. Potilaat, joilla LVEF oli ennen kantasoluhoitoa alle mediaaniarvon (≤62.5%), hyötyivät kantasoluhoidosta enemmän kuin potilaat, joilla LVEF oli yli mediaanin. Myös natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso infarktin jälkeen oli yhteydessä suurempaan LVEF:n paranemiseen BMC-potilailla. Natriureettisten peptidien ja tulehdusmerkkiaineiden pitoisuuksien muutoksissa kantasoluhoidon jälkeen ei kuitenkaan todettu eroa BMC- ja kontrolliryhmän välillä. Sydämen diastolisen toiminnan havaittiin paranevan enemmän BMC-ryhmässä kuin kontrolliryhmässä. Lisäksi BMC-ryhmässä havaittiin lievää laskua keuhkovaltimopaineessa, kun taas kontrolliryhmässä se nousi merkittävästi. In vitro-tutkimukset luuytimestä erilaistetuilla mesenkymaalisilla kantasoluilla puolestaan osoittivat, että tuumorinekroositekijä alfa (TNF-α)-altistus lisäsi solujakautumista ja monien immunosupressiivisten proteiinien tuottoa soluissa. Matala LVEF sekä natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso sydäninfarktin jälkeen kuvaavat infarktivaurion aiheuttamien hemodynaamisten ja neurohumoraalisten reaktioiden vakavuutta, ja tässä tutkimuksessa niiden osoitettiin olevan vahvasti yhteydessä äkillisen ST-nousuinfarktin jälkeen annetun kantasoluhoidon hyötyyn. Kantasoluhoito saattaa myös suojata infarktipotilaita haitalliselta keuhkovaltimopaineen nousulta ja parantaa sydämen diastolista toimintaa. Tulehdusvälittäjäaine TNF-α näytti in vitro-kokeiden perusteella lisäävän luuytimen mesenkymaalisten kantasolujen jakautumista ja aktivoivan niissä monia immunosuppressiivisia puolustusmekanismeja tulehdusta vastaan
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Borges, João Batista. "Regional Lung Kinetics of Ventilator-Induced Lung Injury and Protective-Ventilation Strategies Studied by Dynamic Positron Emission Tomography." Doctoral thesis, Uppsala universitet, Hedenstiernalaboratoriet, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-230022.
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Mechanical ventilation in itself can harm the lung and cause ventilator-induced lung injury (VILI), which can induce or aggravate acute respiratory distress syndrome (ARDS). Much debate remains over pivotal concepts regarding the pathophysiology of VILI, especially about the precise contribution, kinetics, and primary role of potential VILI mechanisms. Consequently, it remains largely unknown how best to design a well-timed and full-bodied mechanical ventilation strategy. Little is known also about small airways dysfunction in ARDS. Dynamic positron emission tomography (PET) with [18F]fluoro-2-deoxy-D-glucose (18F-FDG) can be used to image cellular metabolism, which during lung inflammation mainly reflects neutrophil activity, allowing the study of regional lung inflammation in vivo. We studied the regional evolution of inflammation using dynamic PET/CT imaging of 18F-FDG in VILI and during different lung-protective mechanical ventilation strategies. By dynamic CT we investigated also the location and magnitude of peripheral airway closure and alveolar collapse under high and low distending pressures and high and low inspiratory oxygen fraction. Piglets were submitted to an experimental model of early ARDS combining repeated lung lavages and injurious mechanical ventilation. The animals were subsequently studied during sustained VILI, or submitted to distinct approaches of lung-protective mechanical ventilation: the one recommended by the ARDS Network (ARDSNet), or to one defined as open lung approach (OLA). The normally and poorly aerated regions - corresponding to intermediate gravitational zones - were the primary targets of the inflammatory process accompanying early VILI, which may be attributed to the small volume of the aerated lung that receives most of ventilation. The ARDSNet strategy did not attenuate global pulmonary inflammation during 27h and led to a concentration of inflammatory activity in the upper and poorly aerated lung regions. The OLA, in comparison with the ARDSNet approach, resulted in sustained and better gas exchange and lung mechanics. Moreover, the OLA strategy resulted in less global and regional inflammation. Dynamic CT data suggested that a significant amount of airway closure and related reabsorption atelectasis occurs in acute lung injury. Whether potential distal bronchioles injury (“bronchiolotrauma”) is a critical and decisive element in ventilator-associated lung injury is a matter for future studies.
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Petroni, Ricardo Costa. "Papel da solução salina hipertônica (NaCl 7,5%) no remodelamento pulmonar da endotoxemia induzida por lipopolissacarídeos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5165/tde-03122013-105443/.
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Sepse é uma resposta inflamatória inapropriada desencadeada pela presença de bactérias e/ou produtos bacterianos como lipopolissacarídeos (LPS). A sepse grave e o choque séptico estão associados a taxas de mortalidade de 40 a 60%. A falência respiratória está entre as mais frequentes complicações da sepse grave, ocorrendo em quase 80% dos casos. Cerca de 40% dos pacientes com sepse desenvolvem a síndrome do desconforto respiratório agudo (SDRA), caracterizada principalmente pela alteração da função respiratória, surgimento de edema intersticial pulmonar e deposição de colágeno nos pulmões. Embora a reposição volêmica seja normalmente utilizada em pacientes sépticos, não há consenso quanto ao volume a ser administrado, sendo atualmente recomendada a utilização de pequenos volumes. Neste contexto, a solução salina hipertônica (NaCl 7,5%, SH) tem sido apresentada como um potencial agente terapêutico. Visando contribuir para o conhecimento dos benefícios da solução salina hipertônica (SH) na sepse, o presente trabalho teve como objetivo avaliar a ação do tratamento precoce e tardio com solução hipertônica no pulmão de ratos endotoxêmicos. Ratos Wistar foram separados em 4 grupos (n=10): CTL (sem nenhum insulto ou tratamento); LPS (injetados com LPS 10mg/Kg i.p); HIPER (animais que receberam tratamento com solução hipertônica 7,5% NaCl i.p na dose de 4ml/Kg 15 min. ou 1,5 horas após injeção de LPS) e SALINA ((animais que receberam tratamento com solução salina 0,9% NaCl i.p na dose de 34ml/Kg 15 min. ou 1,5 horas após injeção de LPS). Foram avaliados a mortalidade, e após 24 horas o edema e a mecânica pulmonar, os colágenos tipo I e tipo III, a expressão e atividade da MMP-9, a expressão de FAK e a síntese de óxido nítrico (NO). Nossos resultados mostraram que o tratamento precoce com solução hipertônica evitou a morte dos animais endotoxêmicos. Nenhum dos tratamentos modulou os mediadores inflamatórios. O tratamento precoce com solução hipertônica diminuiu a síntese de iNOS e nitrito, a expressão e atividade de MMP-9 e de FAK, junto com a deposição de colágeno tipo I evitando a substituição do colágeno III. Observamos melhora dos parâmetros de mecânica respiratória. O tratamento tardio com solução hipertônica não apresentou os mesmos resultados promissores observados no tratamento precoce, sugerindo que o tempo de administração da hipertônica é de grande importância para obtenção de seus efeitos terapêuticosSepsis syndrome is caused by inappropriate immune activation due to bacteria and bacterial components released during infection. The respiratory failure is among the most frequent complication of severe sepsis, occurring in almost 80% of the cases. About 40% of septic patients develop acute respiratory distress syndrome (ARDS) which is characterized mainly by the change of respiratory function, interstitial lung edema and fibronectin and collagen deposition in the lung. Fluid resuscitation is normally used in the management of patients with severe sepsis and septic shock. Hypertonic saline solution (HS, NaCl 7,5%) has shown to modulates immune function and decrease pulmonary injury triggered by endotoxemic shock. Our objective was to investigate the effects of early and later HS treatment on the mechanism involved in pulmonary injury, in an experimental model of endotoxemic shock. Wistar rats received lipopolysaccharide - LPS (10mg/kg i.p.) and volume i.v. after 15 minutes (early) or 1,5 hours (later). The animals were assigned in four groups (n=10): control group (not subjected to LPS); LPS group (injected with LPS 10mg/kg i.p); HS group (treated with hypertonic saline, 4 mL/Kg i.v. after LPS) and NS group (treated with normal saline, 34 mL/kg i.v. after LPS). We evaluated mortality and at 24h after treatment, pulmonary edema and mechanics, type I and type III collagen expression, metalloproteinase 9 expression and activity, focal adhesion kinase (FAK) and nitric oxide (NO) synthesis were measured. In the early treatment NS increased pulmonary resistance and elastance, compared to other groups. HS inhibited collagen expression compared to LPS and NS groups and prevented pulmonary injury by decreasing MMP-9 activity in tissue. Expression of FAK was decreased in HS groups compared to LPS and NS groups. NO expression was decreased in HS group, compared to LPS and NS groups. The later treatment with HS did not showed improvement of previous parameters increasing mortality and pulmonary injury. We concluded that HS treatment of endotoxemic shock at the earliest possible time point maximizes its efficacy in preventing pulmonary injury probably acting on nitric oxide-induced FAK activation pathway, which could modulate the collagen deposition in pulmonary tissue, and consequently decrease the progression of pulmonary fibrosis. Later treatment with HS decreased beneficial effects of hypertonic saline observed in early infusion, showed the importance of timing in the result of fluid therapy
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Bernard, Amandine. "Expression des formes membranaire et soluble (Delta 6) de CD127, chaîne alpha du récepteur à l’IL-7, chez le macaque rhésus sain ou infecté par le virus de l’immunodéficience simienne." Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015PA05T008.
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L'interleukine 7 (IL-7) est une cytokine indispensable au développement et à l'homéostasie des lymphocytes T. Le récepteur à l'IL-7 (IL-7R) est composé de la chaîne alpha (ou CD127) partagée avec le récepteur au TSLP et de la chaîne commune gamma c (ou CD132) partagée avec plusieurs récepteurs de cytokines gamma. L'expression de son récepteur a été décrite dans les lymphocytes T, mais n'a pas été clairement démontrée dans les cellules présentatrices d'antigène (CPA). Cependant, l'expression de CD127 et des récepteurs aux cytokines gamma ont été décrits sur ces cellules suggérant l'expression d'un IL-7R fonctionnel par les CPA. De façon intéressante, la chaîne CD127 existe également sous différentes formes solubles (CD127s) résultant d'épissages alternatifs de l'ARN messager. Toutefois, l'expression et la régulation de l'expression des isoformes de CD127 ont été peu étudiées dans les CPA. Par ailleurs, des polymorphismes du gène CD127 ont été identifiés et associés à une forte concentration plasmatique de la forme soluble CD127s ∆6 chez l'Homme et à une plus forte susceptibilité de développer des maladies auto-immunes. Certains de ces polymorphismes ont également été associés à une évolution plus rapide vers le stade SIDA chez les patients HIV. Enfin, sa capacité à lier l'IL-7 suggère un rôle important de cette forme soluble dans la régulation de la réponse à l'IL-7 en agissant sur sa biodisponibilité. Cependant, l'expression de CD127s plasmatique est très controversée chez les patients HIV en phase chronique. De plus, son expression n'est pas connue dans les organes infectés et n'a jamais été décrite en phase aiguë de l'infection. Enfin, son origine et sa fonction ne sont pas encore élucidées. La quantification spécifique de CD127s ∆6 par RT-qPCR chez le macaque rhésus sain révèle une expression minoritaire de CD127s ∆6 dans les PBMC, faible dans les intestins, plus importante dans les ganglions et encore plus importante dans les poumons. De façon plus précise, cette étude met en évidence sur cellules isolées du sang et de la rate de singes sains, une faible expression de CD127 par les monocytes caractérisée néanmoins par une représentation majeure de la forme soluble contrairement aux lymphocytes T. Ces résultats ont été confirmés par la suite in vitro dans 2 populations immunitaires majoritaires des poumons : les macrophages alvéolaires primaires (MA) issus de lavages broncho-alvéolaires (LBA) de macaque rhésus sains et les cellules épithéliales pulmonaires (CEP) humaines de la lignée NCI-H226. Dans une deuxième partie, la quantification spécifique de CD127s ∆6 par RT-qPCR dans les organes (ganglions et poumons) et le dosage de la protéine CD127s plasmatique en phase aiguë de l'infection SIVmac251 révèlent une augmentation significative de son expression dans les poumons aux temps J7, J10 et J14 post infection et de sa concentration plasmatique à J10 chez les singes infectés. Enfin dans une dernière partie, la charge virale et l'IL-7 endogène ont également été mesurées chez les singes infectés afin de mieux comprendre les mécanismes de régulation de l'expression de CD127s ∆6 au cours de l'infection par le SIVmac251. De façon surprenante, aucune corrélation n'a été trouvée entre l'expression de CD127s ∆6 et la charge virale ou l'expression d'IL-7 endogène chez les singes infectés et les singes sains après injection d'une dose pharmacologique d'IL-7. Ces données suggèrent un effet indirect de l'IL-7 et du virus sur l'expression de CD127s ∆6 et un rôle des facteurs de l'inflammation dans la régulation de son expression. Dans l'objectif de mieux définir ces mécanismes de régulation, les transcrits codant pour la forme soluble ont été quantifiés dans les MA et les CEP in vitro après 6H de stimulation ou non sous IL-7 ou TSLP (ligands de CD127) seul ou couplé au TNFα (cytokine pro inflammatoire). (...)Interleukin-7 (IL-7) is a crucial cytokine for T-cell development and peripheral T-cell homeostasis. The IL-7 receptor (IL-7R) is composed by the alpha chain (or CD127) shared with the TSLP receptor and the common gamma chain (or CD132) shared with several receptors of gamma cytokines. IL-7R expression was described in T lymphocytes but was not clearly demonstrated in antigen presenting cells (APC). However, CD127 chain and gamma cytokine receptors were described in these cells suggesting a functional IL-7R expression in APC. Interestingly, the CD127 chain also exists under various soluble forms (CD127s) resulting in alternative splicing of CD127 mRNA. However, the expression and the regulation of CD127 isoforms expression have been barely studied in APC. Moreover, polymorphisms in CD127 gene were identified and associated with a strong plasmatic concentration of the soluble form CD127s ∆6 in Humans and a stronger susceptibility to develop autoimmune diseases. Some of these polymorphisms are also associated with a faster evolution to the AIDS stage for HIV patients. Finally, the capacity of this soluble form to bound IL-7 suggests an important role of CD127s ∆6 to regulate IL-7 response by acting on his availability. However, the plasmatic CD127s expression is very controversial in HIV patients in chronic phase of infection. Moreover it expression was not known in infected organs and has never been described in acute phase of infection. Finally, nobody defines its origin and its function yet. The specific quantification of CD127s ∆6 by RT-qPCR revealed a minority expression of CD127s ∆6 in PBMC, weak in gut, more important in ganglions and even more in lung. More precisely, this study highlight on isolated cells from healthy monkey’s blood and spleen, a weak expression of CD127 by monocytes characterized by a majority expression of the soluble form contrary to T lymphocytes. Afterwards, we confirmed these results in vitro in two major immune populations in lung: in primary alveolar macrophages (AM) isolated from broncho-alveolar lavages (BAL) from healthy rhesus monkey and in the NCI-H226 lineage of human lung epithelial cells (LEC). In a second part, the specific quantification of CD127s Δ6 by RT-qPCR in organs (ganglions and lung) and the determination of the CD127s plasmatic protein at the acute phase of SIVmac251 infection revealed a significant up-regulation of this expression in lung in times D7, D10 and D14 post infection and its plasmatic concentration at D10 in infected monkeys. Finally, in the last part, we also quantified the viral load and IL-7 expression from infected monkeys to understand mechanisms implicated in regulation of CD127 expression during SIVmac251 infection. Surprisingly, we found none correlation between CD127s ∆6 expression and viral load or IL-7 expression from infected monkeys and healthy monkeys after injection of a pharmacological dose of IL-7. These data suggest an indirect effect of IL-7 and virus on CD127s ∆6 expression and a role of inflammation factors in regulation of his expression. In order to better define these mechanisms of regulation, the transcripts coding for the soluble form were quantified on AM and LEC in vitro after 6H of stimulation with or without IL-7 or TSLP (ligands of CD127) alone or combined with TNFα (pro inflammatory cytokine). Surprisingly, contrary to T lymphocytes, IL-7 do not induces down regulation of CD127 expression on AM and LEC. Nevertheless, CD127s ∆6 expression is upregulated upon TNFα by AM in a dose dependent manner. Moreover, the costimulation (IL-7 + TNFα) induces CD127s ∆6 expression by LEC revealing a synergic effect of IL-7 and TNFα. Finally the polarization of macrophages derived from human monocytes (hMDM) show that activated state of macrophages impact not only expression but also regulation of CD127 expression by these cytokines. (...)
7
Melo, Adriana Corrêa. "Função pulmonar, estresse oxidativo e marcadores inflamatórios na lesão pulmonar aguda induzida por lipopolissacarídeo: diferentes efeitos da atorvastatina, pravastatina e simvastatina." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5985.
Full textAbstract:
Nosso objetivo foi determinar que tipo de estatina pode atenuar a lesão pulmonar aguda (LPA) induzida por lipopolissacarídeo (LPS) em camundongos da linhagem C57Bl/6. Trinta camundongos machos ( 23 g) foram divididos em 5 grupos (n=6 cada): grupo LPS (10 mg/kg) administrado intraperitonealmente (i.p.), LPS mais atorvastatina (10 mg/kg/dia; grupo LPS+A), LPS mais pravastatina (5 mg/kg/dia; grupo LPS+P) e LPS mais sinvastatina (20 mg/kg/dia; grupo LPS+S). O grupo controle recebeu salina i.p.. Em um grupo separado de camundongos (n=5), a soma das pressões pulmonares resistivas e viscoelásticas (DeltaPtot) e elastância estática (E[st]) foram medidas. Um dia após a administração de LPS os camundongos foram sacrificados (24 h) por deslocamento cervical e logo em seguida foi realizado lavado broncoalveolar (LBA). Os pulmões foram removidos para análise histopatológica e homogeneizados para análises bioquímicas (ELISA, catalase, superóxido dismutase, mieloperoxidase, substâncias reativas ao ácido tiobarbitúrico, carbonilação de proteínas e método de Griess). A quantidade de leucócitos foi menor no grupo LPS+P (p<0,01) e LPS+S (p<0,05) em comparação ao grupo LPS. Os níveis de MCP-1 e IL-6 reduziram no grupo LPS+P (p<0,01), enquanto o grupo LPS + S mostrou redução apenas nos níveis de IL-6 (p<0,05) em comparação ao grupo LPS. Marcadores redox (superóxido dismutase e catalase) foram menores no grupo LPS+A (p<0,01) em comparação ao grupo LPS. A peroxidação lipídica (malondialdeído e hidroperóxidos) diminuiu em todos os grupos tratados (p<0,05) quando comparados ao grupo LPS. A mieloperoxidase foi menor no grupo LPS+P (p<0,01) quando comparado ao grupo LPS. DeltaPtot e E(st) foram, significativamente, maiores no grupo LPS do que nos outros grupos. Nossos resultados sugerem que atorvastatina e pravastatina, mas não a sinvastatina, exibiram ações anti-inflamatórias e antioxidantes na LPA induzida por LPS.To determinate what statins could attenuate acute lung injury (ALI) induced by lipopolysaccharide (LPS) in C57BL/6 mice. Young male mice ( 23 g) were divided into 5 groups (n=6 each): injected with LPS i.p. (10 mg/kg), LPS plus atorvastatin (10 mg/kg/day; LPS+A group) or pravastatin (5 mg/kg/day; LPS+P group) or simvastatin (20 mg/kg/day; LPS+S group). Control group received saline (i.p.). In a separated group of mice (n=5) the sum of pulmonary resistive and viscoelastic pressures (DeltaPtot) and static elastance (E[st]) were measured. One day later (24 h), the animals were sacrificed, BAL performed and lungs were removed for histopathological analysis and homogenized for biochemical analyses (ELISA, catalase, superoxide dismutase, myeloperoxidase, thiobarbituric acid reactive substances, protein carbonyls and griess assay). The amount of leukocytes was lower in LPS+P (p<0.01) and LPS+S (p<0.05). Cytokine levels of MCP-1 was lower in LPS+P (p<0.01) while IL-6 was lower in LPS+P (p<0.01) and LPS+S (p <0.05). Redox markers (superoxide dismutase and catalase) were lower in LPS+A (p<0.01). Lipid peroxidation (malondialdehyde and hydroperoxides) were lower in all treated groups (p<0.05). Myeloperoxidase was lower in LPS+P (p<0.01). DeltaPtot and E(st) were significantly higher in the LPS group than in the other groups. Our results suggest that atorvastatin and pravastatin, but no simvastatin, exhibits anti-inflammatory and antioxidant actions in LPS-induced ALI.
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Monsel, Antoine. "Inflammation aiguë pulmonaire en réanimation : développement d'axes diagnostiques, préventifs et de thérapies immunomodulatrices." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066248/document.
Full textAbstract:
Les deux formes d'inflammation pulmonaire en réanimation sont la pneumonie et le syndrome de détresse respiratoire aiguë (SDRA). Nous avons conçu un test diagnostique rapide basé sur l'autofluorescence des neutrophiles alvéolaires. S'appuyant sur une étude expérimentale, puis sur une étude clinique randomisée, nous avons montré que les sondes d'intubation avec ballonnets coniques diminuaient les micro-inhalations sans prévenir l'incidence des pneumonies post-opératoire. Une grande variabilité des pressions des ballonnets coniques pose la question de leur effet délétère. La thérapie cellulaire basée sur les cellules souches mésenchymateuses (CSM) est prometteuse. L'étude des effets thérapeutiques des vésicules extracellulaires issues de CSM (VE-CSM) constitue un nouvel axe de recherche. Dans 2 modèles murins de SDRA, puis dans un modèle de poumons humains ex vivo, nous avons démontré des effets thérapeutiques des VE-CSM. Nous avons ensuite étudié les lymphocytes T régulateurs (Treg) pulmonaires et systémiques dans le SDRA. Cette étude a montré un déficit quantitatif plutôt que fonctionnel de la population Treg pulmonaire dans le SDRA, avec une cinétique évoquant un recrutement des Treg circulants vers le compartiment pulmonaire au cours de la maladie. En conclusion, nos travaux ont développé de nouvelles stratégies diagnostiques et préventives des pneumonies de réanimation, afin de réduire leur impact en termes de morbi-mortalité. Les bénéfices thérapeutiques des CSM et des VE-CSM dans le SDRA expérimental, ainsi que l'altération du phénotype Treg observé chez nos patients, ouvrent de nouveaux champs de recherche vers le développement d'immunothérapies innovantesPneumonia and acute respiratory distress syndrome (ARDS) are two facets of severe acute lunginflammation, often met in intensive care unit (ICU). Rapid diagnosis of pneumonia remains essential inorder to optimize their management. We worked on setting up a quick test diagnosis based on theintensity of alveolar neutrophils autofluorescence. The validation of this test in a multicenter cohort isunderway. Preventing microaspiration across the cuff remains a priority to prevent pneumonia inmechanically ventilated patients. Based on the results of an ex vivo study followed by a clinicalrandomized trial, we showed that tapered-cuff endotracheal tube prevented microaspiration in the exvivo model, without lowering intraoperative microaspirations and postoperative pneumonia rate aftermajor vascular surgery. Both studies yielded similar results concerning the higher variation of cuffpressureover time, which leads to the question of their safety of use in terms of potential resultingtracheal wall ischemia.Pneumonia represents 80% of the cause of ARDS, which can be viewed as lung uncontrolledinflammatory response. Cell-based therapy using mesenchymal stem cells (MSC) is a growing field ofresearch in ARDS therapy. Despite numerous beneficial effects in ARDS, their capacity of self-renewalpoints them out as a potential cancer inducer in the mid-long term. In this context, evaluating thetherapeutic effects of extracellular vesicles-released from MSC (EV-MSC) represents a novel approach.We showed therapeutic effects of EC-CSM in two murine model of ARDS induced by endotoxin or liveEscherichia coli bacteria, and in another ex vivo human lung preparation.We then focused our research on temporal and compartmental dynamics of regulatory T cells(Treg) phenotypes in ARDS patients. This prospective observational clinical study showed that Early ARDSwas characterized with an alveolar compartment fully polarized towards pro-inflammatory state andneutrophils chemotaxis. In lung compartment, and compared to control patients, ARDS patients showeda quantitative Tregs deficiency, which partially recovered over time, while activation markers wereoverexpressed in both Tregs and effectors T cells (Teff). Conversely, patients with ARDS had a higherproportion of systemic Tregs compared to controls. Significant increased proportion in circulating Th1,Th22, and ILC1 subsets, and decreased proportion in ILC3 subsets were also found in ARDS patientscompared to controls.In conclusion, we developed novel strategies to diagnose and prevent pneumonia in ICU, whichremains essential to improve patients’ outcomes. Therapeutic effects of MSC and EV-MSC, as well asTreg phenotype alterations pave the way for development of novel immunoregulatory therapies
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Holms, Carla Augusto Thomaz de Aquino. "Avaliação da resposta inflamatória pulmonar de suínos submetidos a lesão pulmonar aguda induzida por ácido clorídrico e tratados com solução salina hipertônica." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-22012013-174923/.
Full textAbstract:
INTRODUÇÃO: A lesão pulmonar aguda (LPA) decorrente de aspiração do conteúdo gástrico é freqüente em pacientes com nível de consciência comprometido e depressão dos reflexos de vias aéreas. A solução salina hipertônica (HS) a 7,5% apresenta resultados ainda controversos quanto ao seu potencial efeito protetor na resposta inflamatória pulmonar. OBJETIVOS: Este estudo teve como objetivo avaliar o potencial efeito antiinflamatório da solução salina hipertônica no modelo experimental de lesão pulmonar por aspiração de ácido clorídrico (HCl). MÉTODOS: Foram utilizados 32 suínos (n=32; 8/grupo) divididos aleatoriamente nos seguintes grupos: Sham, onde os animais foram somente anestesiados, ventilados e observados; HS, onde os animais receberam infusão de HS a 7,5% (4 ml/kg), sem LPA; ALI, onde os animais foram submetidos à LPA com HCl; ALI+HS, onde os animais foram submetidos à LPA com HCl e tratados com HS a 7,5% (4 ml/kg). Foram mensurados parâmetros hemodinâmicos e ventilatórios. Amostras de sangue foram coletadas para hemogasometria e análise dos níveis plasmáticos de TNF-?. Foram coletadas amostras do lavado broncoalveolar para mensuração das seguintes citocinas: IL-1, IL-6, IL-8, IL-10 e TNF-?, e realização do burst oxidativo das células pulmonares. O tecido pulmonar foi coletado para análise histológica posterior. A análise estatística foi realizada pela análise de variância com medidas repetidas (ANOVA) seguida por teste de Tukey. O grau de significância estabelecido foi de 5% (p<0,05). RESULTADOS: Houve diferença estatística significante quanto aos parâmetros ventilatórios, oxigenação sanguinea, burst oxidativo e análise histológica pulmonar dos grupos ALI e ALI+HS, quando comparados aos grupos Sham e HS. Níveis de IL-6 e IL-8 apresentaram-se mais elevados nos grupos ALI e ALI+HS, porém sem diferença estatística entre grupos. CONCLUSÃO: O modelo de LPA estudado foi capaz de promover lesão pulmonar direta e heterogênea, porém o grupo tratado com solução salina 7,5% não apresentou diferença estatística sobre o grupo não tratado no que alude aos parâmetros avaliados.BACKGROUND: Acute lung injury (ALI) caused by aspiration of gastric contents is not ununsual in patients with depression of airway reflexes. The potential anti-inflammatory effects of hypertonic saline 7.5% (HS) is still controversial on pulmonary response. OBJECTIVES: This study aimed to evaluate the potential anti-inflamatory effect of hypertonic saline (HS) in a swine model of hydrochloric acid (HCl) aspiration. METHODS: 32 pigs (n=32; 8/group) were randomly divided into the following groups: Sham, the animals were only anesthetized, ventilated and observed; HS, the animals received an 7.5% hypertonic saline infusion (4ml/kg); ALI, animals were submitted to ALI with HCl infusion; ALI+HS, animals were submitted to ALI with HCl infusion and treated with 7.5% hypertonic saline (4ml/kg). Hemodynamic and ventilatory parameters were measured. Blood samples were collected for blood gas analysis and plasma levels mensuration of TNF-?. Bronchoalveolar samples were also collected for IL-1, IL-6, IL-8, IL-10 and TNF-? cytokine mensuration and oxidative burst analysis. Lung tissue was collected for histological analysis. A parametrical analysis of variance with repeated measurement (ANOVA) followed by Tukey test was done. The significance level was set at 5% (p<0,05). RESULTS: There were estatistical differences regarding to ventilatory parameters, oxigenation, oxidative burst and pulmonary histological evaluation in ALI and ALI+HS groups, when compared to Sham and HS. IL-6 and IL-8 levels were higher in ALI and ALI+HS groups. However, no statistical difference were found between groups. CONCLUSION: The ALI model was effective to promote diffuse and heterogeneous lung injury. However, the group treated with 7.5% hypertonic saline did not presented statistical difference when compared to the non treated group regarding the evaluated parameters.
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Junior, Luciano Filgueiras Ribeiro. "O eixo LTB4/MYD88 na inflamação estéril e na sepse em modelos experimentais de diabetes." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-25112014-165209/.
Full textAbstract:
A diabetes tipo 1 (DT1) está associada `a inflamação estéril (IE) e maior susceptibilidade a sepse. A sepse induz a síndrome da resposta inflamatória sistêmica (SIRS) e a inflamação pulmonar aguda (ALI). O leucotrieno (LT) B4 produzido condições inflamatórias induz a expressão de MyD88 em macrófagos (MA). Hipotetizamos que a DT1 induz a síntese de LTB4 promovendo a IE e isto contribui para SIRS, susceptibilidade a sepse e ALI. Os diabéticos apresentaram níveis elevados de LTB4 e IL-1b no soro e seu MA expressaram mais MyD88/STAT-1. A expressão de STAT-1 foi induzida por c-Jun de forma dependente de LTB4. O tratamento com insulina restaurou os níveis de LTB4 e STAT-1/MyD88 e a inibição de LTB4 restaurou os níveis de MyD88 e IL-1b. Na sepse, a inibição de 5LO prolongou a sobrevida dos diabéticos e diminuiu a SIRS menos IL-1b e IL-10 no soro e TNF-a e IL-1b na cavidade peritoneal. O pulmão dos diabéticos apresentaram ALI menos intensa que se correlacionou com um altos níveis de SOCS-1, baixos níveis de MyD88 e falha na ativação de NFkB nos macrófagos alveolares.Type 1 diabetes (T1D) is associated with sterile inflammation (SI) and increased sepsis susceptibility. Sepsis induces Systemic Inflammatory Response Syndrome (SIRS) and Acute Lung Injury (ALI). Leukotriene (LT) B4 is produced in inflammatory conditions and induces MyD88 expression in macrophages (MA). We hypothesized that T1D induce LB4 that promotes SI contributing to SIRS, sepsis susceptibility and ALI. Diabetics presented higher levels of LTB4 and e IL-1b in the serum and MA expressed more MyD88/STAT-1. STAT-1 expression was induced by c-Jun on LTB4 dependent manner. Insulin treatment restored LTB4 and STAT-1/MyD88 levels and inhibition of LTB4 restored MyD88 and IL-1b levels. During sepsis, 5LO inhibition increased diabetics survival and inhibited SIRS- lower levels of IL-1b and IL-10 in the serum and TNF-a and IL-1b in the peritoneal cavity. Lungs from diabetics presented milder ALI that correlated with high levels of SOCS-1, low levels of MyD88 and impaired NFkB activation in alveolar macrophages.
Books on the topic "Pulmonary acute inflammation"
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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.
Full textAbstract:
The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0036.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among troponin-negative subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
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Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_001.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
4
Giannitsis, Evangelos, and Hugo A. Katus. Biomarkers in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0036_update_002.
Full textAbstract:
Biomarker testing in the evaluation of a patient with acute chest pain is best established for cardiac troponins that allow the diagnosis of myocardial infarction, risk estimation of short- and long-term risk of death and myocardial infarction, and guidance of pharmacological therapy, as well as the need and timing of invasive strategy. Newer, more sensitive troponin assays have become commercially available and have the capability to detect myocardial infarction earlier and more sensitively than standard assays, but they are hampered by a lack of clinical specificity, i.e. the ability to discriminate myocardial ischaemia from myocardial necrosis not related to ischaemia such as myocarditis, pulmonary embolism, or decompensated heart failure. Strategies to improve clinical specificity (including strict adherence to the universal myocardial infarction definition and the need for serial troponin measurements to detect an acute rise and/or fall of cardiac troponin) will improve the interpretation of the increasing number of positive results. Other biomarkers of inflammation, activated coagulation/fibrinolysis, and increased ventricular stress mirror different aspects of the underlying disease activity and may help to improve our understanding of the pathophysiological mechanisms of acute coronary syndromes. Among the flood of new biomarkers, there are several novel promising biomarkers, such as copeptin that allows an earlier rule-out of myocardial infarction in combination with cardiac troponin, whereas MR-proANP and MR-proADM appear to allow a refinement of cardiovascular risk. GDF-15 might help to identify candidates for an early invasive vs conservative strategy. A multi-marker approach to biomarkers becomes more and more attractive, as increasing evidence suggests that a combination of several biomarkers may help to predict individual risk and treatment benefits, particularly among normal-troponin subjects. Future goals include the acceleration of rule-in and rule-out of patients with suspected acute coronary syndrome, in order to shorten lengths of stay in the emergency department, and to optimize patient management and the use of health care resources. New algorithms using high-sensitivity cardiac troponin assays at low cut-offs alone, or in combination with additional biomarkers, allow to establish accelerated rule-out algorithms within 1 or 2 hours.
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Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.
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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household pollution from cooking fuels may cause up to two million premature deaths per year in the developing world. The hazards of black smoke air pollution have been known since antiquity. The first descriptions of deaths caused by air pollution are those recorded after the eruption of Vesuvius in ad 79. In modern times, the infamous smogs of the early twentieth century in Belgium and London were clearly shown to trigger deaths in people with chronic bronchitis and heart disease. In mechanistic terms, black smoke and sulphur dioxide generated from industrial processes and domestic coal burning cause airway inflammation, exacerbation of chronic bronchitis, and consequent heart failure. Epidemiological analysis has confirmed that the deaths included both those who were likely to have died soon anyway and those who might well have survived for months or years if the pollution event had not occurred. Clean air legislation has dramatically reduced the levels of these traditional pollutants in the West, although these pollutants are still important in China, and smoke from solid cooking fuel continues to take a heavy toll amongst women in less developed parts of the world. New forms of air pollution have emerged, principally due to the increase in motor vehicle traffic since the 1950s. The combination of fine particulates and ground-level ozone causes ‘summer smogs’ which intensify over cities during summer periods of high barometric pressure. In Los Angeles and Mexico City, ozone concentrations commonly reach levels which are associated with adverse respiratory effects in normal and asthmatic subjects. Ozone directly affects the airways, causing reduced inspiratory capacity. This effect is more marked in patients with asthma and is clinically important, since epidemiological studies have found linear associations between ozone concentrations and admission rates for asthma and related respiratory diseases. Ozone induces an acute neutrophilic inflammatory response in both human and animal airways, together with release of chemokines (e.g. interleukin 8 and growth-related oncogene-alpha). Nitrogen oxides have less direct effect on human airways, but they increase the response to allergen challenge in patients with atopic asthma. Nitrogen oxide exposure also increases the risk of becoming ill after exposure to influenza. Alveolar macrophages are less able to inactivate influenza viruses and this leads to an increased probability of infection after experimental exposure to influenza. In the last two decades, major concerns have been raised about the effects of fine particulates. An association between fine particulate levels and cardiovascular and respiratory mortality and morbidity was first reported in 1993 and has since been confirmed in several other countries. Globally, about 90% of airborne particles are formed naturally, from sea spray, dust storms, volcanoes, and burning grass and forests. Human activity accounts for about 10% of aerosols (in terms of mass). This comes from transport, power stations, and various industrial processes. Diesel exhaust is the principal source of fine particulate pollution in Europe, while sea spray is the principal source in California, and agricultural activity is a major contributor in inland areas of the US. Dust storms are important sources in the Sahara, the Middle East, and parts of China. The mechanism of adverse health effects remains unclear but, unlike the case for ozone and nitrogen oxides, there is no safe threshold for the health effects of particulates. Since the 1990s, tax measures aimed at reducing greenhouse gas emissions have led to a rapid rise in the proportion of new cars with diesel engines. In the UK, this rose from 4% in 1990 to one-third of new cars in 2004 while, in France, over half of new vehicles have diesel engines. Diesel exhaust particles may increase the risk of sensitization to airborne allergens and cause airways inflammation both in vitro and in vivo. Extensive epidemiological work has confirmed that there is an association between increased exposure to environmental fine particulates and death from cardiovascular causes. Various mechanisms have been proposed: cardiac rhythm disturbance seems the most likely at present. It has also been proposed that high numbers of ultrafine particles may cause alveolar inflammation which then exacerbates preexisting cardiac and pulmonary disease. In support of this hypothesis, the metal content of ultrafine particles induces oxidative stress when alveolar macrophages are exposed to particles in vitro. While this is a plausible mechanism, in epidemiological studies it is difficult to separate the effects of ultrafine particles from those of other traffic-related pollutants.
Book chapters on the topic "Pulmonary acute inflammation"
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An, Gary, Michael Wandling, and Scott Christley. "Agent-Based Modeling Approaches to Multi-Scale Systems Biology: An Example Agent-Based Model of Acute Pulmonary Inflammation." In Systems Biology, 429–61. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6803-1_15.
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Ruigrok, Dieuwertje, and Anton Vonk Noordegraaf. "Pathophysiology of acute pulmonary embolism." In ESC CardioMed, 2756–58. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0657.
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Acute right ventricular (RV) failure and impaired gas exchange (mainly hypoxaemia) can be two important issues clinicians are confronted with in patients with acute pulmonary embolism. An acute increase in RV afterload due to mechanical obstruction and vasoconstriction is the crucial factor starting a cascade with compensatory mechanisms, RV dilatation, RV ischaemia, and inflammation ultimately leading to RV dysfunction/failure. On the other hand, vascular occlusion leads to redistribution of pulmonary perfusion to regions with relative overperfusion causing profound hypoxaemia. Less commonly, shunting occurs due to atelectasis or due to opening of a patent foramen ovale, causing refractory hypoxaemia. Understanding these mechanisms is crucial in making the right treatment decisions when faced with a patient with acute pulmonary embolism and haemodynamic or respiratory instability.
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Tarı Selçuk, Kevser. "Epidemiology of Inflammation-Related Diseases." In Role of Nutrition in Providing Pro-/Anti-Inflammatory Balance, 24–44. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-3594-3.ch002.
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Inflammation, a vital defense mechanism for health, is defined as the immune system's response to harmful stimuli such as pathogens, damaged cells, toxic compounds or irradiation. Inflammation is usually examined in two groups: acute and chronic. Chronic inflammation instigates various kinds of diseases that cause premature mortality and morbidity such us cardiovascular diseases, cancer, diabetes mellitus (DM), asthma-chronic obstructive pulmonary disease (COPD), obesity, metabolic syndrome (METs), inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), osteoporosis, and neurological diseases via dysregulation of various signaling pathways such as nuclear factor kappa-B (NF-κB), signal transducer, activator of transcription 3 (STAT3), etc. These inflammation-related diseases are among the major causes of mortality and morbidity in almost every region of the world. Studies have shown that these diseases associated with inflammation have tended to increase worldwide.
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Tse, Doris, and Kin-Sang Chan. "Cough and other pulmonary symptoms." In Oxford Textbook of Palliative Medicine, edited by Nathan I. Cherny, Marie T. Fallon, Stein Kaasa, Russell K. Portenoy, and David C. Currow, 604–10. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198821328.003.0059.
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Respiratory symptoms other than breathlessness are prevalent in palliative care patients suffering from cancer or chronic lung disease, including chronic obstructive pulmonary disease, bronchiectasis, and cystic fibrosis. Cough may cause physical and psychological morbidity with impaired quality of life. In chronic obstructive pulmonary disease, chronic cough and sputum are associated with disease progression and poorer prognosis. Recommendations on the symptomatic treatment of cough are based on limited evidence in palliative care settings, expert consensus, and studies involving other patients with chronic cough. Novel antitussive agents are being developed with more understanding of the role of ion channels in cough mechanism. Airway hypersecretion due to chronic inflammation and infection is common in chronic lung disease and the use of mucoactive agents may have a modest benefit on acute exacerbations and quality of life. Massive hypersecretion as in bronchorrhoea is uncommon, but can be distressing with no standard treatment. The choice of managing the patient with malignant pleural effusion includes repeated thoracocentesis, pleurodesis, or an intrapleural catheter, depending on the patient’s predicted survival and other factors. Haemoptysis is often alarming to patients and their families. History taking, physical examination, and a chest radiograph are informative, and guide the treatment plan in most of the patients. Other imaging and invasive interventions should be carefully considered in patients when evaluating whether it is feasible to stop massive bleeding from a localized site.
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Dotto, Annapaola. "The Anesthesiologist Contribution to Management of Acute Pancreatitis." In Multidisciplinary Management of Pancreatitis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105821.
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Acute pancreatitis is a complex disease, and although most patients have a self-limiting illness, a minority of them develop severe disease and may need Intensive Care Unit admission. Regardless of severity degree, two cornerstones of acute pancreatitis multidisciplinary management are: fluid resuscitation and pain relief. These patients are frequently hypovolemic because of decreased oral intake, vomiting, fever, and fluid sequestration associated with pancreatic and systemic inflammation. Early intravenous volume resuscitation seems to reduce pancreatic hypoperfusion and multiorgan failure, but fluid overload has been associated with worse outcome, and maintaining proper hydration could be challenging. Acute pancreatitis is a very painful condition and effective analgesia is one of the priorities. Pain relief has a positive impact because of reduced stress response, sympathetic-induced vasoconstriction, and pulmonary complications. It is suggested to use a multimodal analgesic approach, to achieve patient’s satisfaction, minimize opioid consumption and side effects. A modern and effective approach involves the use of patient-controlled analgesia and thoracic epidural analgesia. We would revise these two items to offer early and better multidisciplinary management to patients with acute pancreatitis, including those with mild to moderate disease, who are managed in general surgical wards, with the aim to improve their outcome and hospital stay.
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Farne, Hugo, Edward Norris-Cervetto, and James Warbrick-Smith. "Cough." In Oxford Cases in Medicine and Surgery. Oxford University Press, 2015. http://dx.doi.org/10.1093/oso/9780198716228.003.0013.
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First, ask open questions about the cough itself: • Acute or chronic? The British Thoracic Society (BTS) defines acute as <3 weeks and chronic as >8 weeks. Between 3 and 8 weeks the cough may be due to recovering acute illness or developing chronic illness. • Constant or intermittent? A cough that is intermittent may suggest an extrinsic trigger (e.g. if the patient only coughs at work there may be an allergy to something in the workplace). A cough that is constant suggests an intrinsic cause. • Productive or dry? The presence of sputum indicates inflammation and/or infection. Patients with chronic obstructive pulmonary disease (COPD) have chronically inflamed airways and often produce white or clear sputum. Patients with infection have yellow or green sputum. Particularly large volumes of sputum, often green or rusty coloured, may be coughed up in bronchiectasis and lung abscesses. • Blood? More specifically: ■ Blood-streaked sputum? Suggests infection or bronchiectasis. ■ Pink and frothy sputum? Suggests pulmonary oedema. ■ Frank blood (haemoptysis)? See Chapter 8. Suggests tuberculosis (TB), lung cancer, pulmonary embolus, bronchiectasis, or other rarer causes (e.g. granulomatosis with polyangiitis (GPA, formerly known as Wegener’s granulomatosis), or Goodpasture’s syndrome). • Timing? Asthma is classically worse at night and early hours of the morning. Pulmonary oedema or gastro-oesophageal reflux disease (GORD) can also be worse at night due to the positional effects of lying flat. Patients often report sleeping propped up on pillows to mitigate these effects. Trigger factors such as pets, cold weather, or exercise indicate asthma, as does a worsening in spring/summer. • Character? A wheezy cough suggests airway obstruction due to asthma or COPD. A bovine cough (breathy) is characteristic of vocal cord paralysis. A dry cough is suggestive of a bronchitis (usually viral) or interstitial lung disease. A gurgling/wet cough is suggestive of bronchiectasis. Pertussis infection causes a ‘whooping’ cough. Second, ask directed questions about factors that might be triggering the cough: • Environmental irritants: Smoking? Occupation? Pets? Change of house, office, etc? • Past medical history: Asthma? GORD? Rhinitis/sinusitis? Heart failure? Recent chest infection? • Drug history? Angiotensin-converting enzyme (ACE) inhibitors in particular can cause a cough.
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Bourke, S. J., and G. P. Spickett. "Hypersensitivity pneumonitis." In Oxford Textbook of Medicine, edited by Pallav L. Shah, 4244–56. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0424.
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Hypersensitivity pneumonitis is an immune-mediated lung disease in which the repeated inhalation of certain antigens provokes a hypersensitivity response, with granulomatous inflammation in the distal bronchioles and alveoli of susceptible people. A diverse range of antigens including bacteria (Thermophilic actinomycetes), fungi (Trichosporon cutaneum), animal proteins (bird antigens), mycobacteria, and chemicals may cause the disease. The commonest forms are bird fancier’s lung, farmer’s lung, humidifier lung, and metal-working fluid pneumonitis. In some cases no antigen is identified. Acute disease is characterized by recurrent episodes of breathlessness, cough, fevers, malaise, and flu-like symptoms occurring 4–8 hours after antigen exposure. Fever and basal crackles are the main physical signs. Chronic disease is characterized by the insidious development of dyspnoea and persistent pneumonitis, sometimes progressing to lung fibrosis. Clinical features are similar to those of other varieties of pulmonary fibrosis, but clubbing is uncommon.
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Little, Brent P., and Travis S. Henry. "Bronchiolitis." In Chest Imaging, 331–36. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780199858064.003.0057.
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In children, the term bronchiolitis refers to an acute respiratory illness caused by bronchiolar infection, typically by respiratory syncytial virus (RSV) or other viruses. In adults, the term refers to a primarily bronchiolar pattern of infection or inflammation caused by many pulmonary infections, systemic inflammatory conditions, inhaled irritants, certain systemic conditions, and accompanying several congenital diseases. Imaging may be helpful to assess the extent and severity of bronchiolitis and to establish a differential diagnosis based on the distribution of imaging findings, their respective morphologies, and any ancillary findings. Presence of cavities or architectural distortion with a bronchiolitis pattern, especially in the upper lungs, should prompt consideration of tuberculosis. Aspiration bronchiolitis is a common finding in patients with severe reflux or with impaired swallowing mechanisms. Early diagnosis of hypersensitivity pneumonitis can lead to prompt identification of the offending antigen. In cases with pure centrilobular nodules, smoking history is paramount – smokers get RB, non-smokers have a higher likelihood of hypersensitivity pneumonitis.
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Daga, Mradul Kumar, Siddharth Chand, Naresh Kumar, Govind Mawari, R. V. Raghu, and J. Aarthi. "Proinflammatory and Thrombotic Manifestations and the Therapeutic Options of COVID-19." In Coronaviruses, 49–78. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815123371123030005.
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COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS CoV 2), has put the global health system into crisis. The complications of the disease include respiratory failure, proinflammatory, and thromboembolic presentations. It is being increasingly recognised that host response with the inflammatory and thrombotic state is responsible for the severity of the disease. Numerous studies are now showing that increased inflammatory markers like interleukin (IL) 6 portray a poor prognosis. Thrombo-embolic complications like pulmonary embolism also produce clinical deterioration in COVID 19. The management of the disease presently includes antiviral, anti-inflammatory, and anticoagulant therapy along with supportive care for respiratory complications. The therapeutic challenge is augmented due to the varied clinical presentations, rapid worsening, and lack of a clear understanding of the pathophysiology. The initial data regarding the treatment options are of low quality and are mostly from cohort analysis. Many randomised controlled trials (RCT) are ongoing, and the results from the RCTs will help in developing better treatment options. We discuss in this review the pathophysiology and mechanism behind the increased inflammation and thrombosis. We will also discuss the available therapeutics options and the recommendations of various guidelines regarding the management of the proinflammatory and thrombotic state.
Conference papers on the topic "Pulmonary acute inflammation"
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Hilliard, Kristie L., Joseph P. Mizgerd, Eri Allen, Matthew R. Jones, and Lee J. Quinton. "The Hepatic Acute Phase Response Regulates Pulmonary Inflammation During Pneumonia." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3277.
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Toumpanakis, Dimitrios, Eleftheria Mizi, Vyronia Vassilakopoulou, Athanasia Chatzianastasiou, Stamatios Theocharis, and Theodoros Vassilakopoulos. "Resistive breathing aggravates pulmonary inflammation and emphysema in experimental models of chronic obstructive pulmonary disease." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.yi04.
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Strahan, Brian, and Patrick Arndt. "S100B Regulates Pulmonary Neutrophil Recruitment In Lipopolysaccharide-induced Acute Lung Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2319.
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Gonzalez-Ferrer, S., H. Peñaloza, A. McCollum, R. Van Der Geest, N. Kohli, M. Tabary, Z. Xiong, et al. "STAT1 Modulates Neutrophilic Inflammation During Acute Pulmonary Infection with Klebsiella Pneumoniae." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2189.
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Shpagina, L. A., E. B. Logashenko, and O. S. Kotova. "ACUTE EXACERBATIONS OF OCCUPATIONAL CHRONIC OBSTRUCTIVE PULMONARY DISEASE DUE TO INDUSTRIAL AEROSOLS CONTAINING." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-593-597.
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Abstract. Phenotypes of exacerbations of occupational chronic obstructive pulmonary disease (COPD) due to aerosols containing nanoparticles is not studied enough. The objective was to establish rate, severity, cellular type of inflammation, clinical features of acute exacerbations of occupational COPD due to industrial aerosols containing nanoparticles exposure. Materials and methods. A prospective observational study of 50 subjects with occupational COPD (of which 26 due to aerosols, containing metal nanoparticles and 24 due to aerosols containing silica nanoparticles) and of 50 subjects with COPD due to tobacco smoke performed. Follow up period was 26 (24; 30) months. Groups were matched by age, gender, COPD duration. Groups of occupational COPD has the same smoking status. Nanoparticles and dust concentrations at workplaces air were measured by inductively coupled plasma atomic emission spectrometry and by scanning electron microscopy. COPD exacerbations rate and severity, cellular type of inflammation during exacerbations were investigated. Relationships were assessed by Cox proportional-hazards regression. Results. Occupational COPD due to aerosols containing metal nanoparticles exposure was characterized by high exacerbation rate. In comparison to occupational COPD due to aerosols containing silica nanoparticles exposure the hazard ratio (HR) was 4,59, 95% CI 1,35–15,63, in relation to COPD in tobacco smokers HR was 3,35, 95% CI1,22 – 9,21. The risk of exacerbations requiring hospitalization also was higher in this group, HR 4,35, 95% CI 1,10-12,3 and HR 3,90, 95% CI 1,33–11,42, respectively. In occupational COPD due to aerosols containing silica nanoparticles the exacerbation rate was the least. Metal nanoparticles mass concentration at the workplace air was associated with COPD exacerbations HR 1,031, 95% CI 1,012–1,11, exacerbations requiring hospitalization HR 1,028, 95% CI 1,010–1,092 and with eosinophilic inflammation during COPD exacerbation ОР 0,015, 95% CI 0,002 – 0,036. Silica nanoparticles mass concentration was associated with COPD exacerbations HR 0,025, 95% CI 0,003–0,094, exacerbations requiring hospitalization HR 0,021, 95% CI 0,009–0,105 and with neutrophilic inflammation during COPD exacerbation HR 1,019, 95% CI 1,008–1,057. Exacerbations of occupational COPD due to aerosols containing nanoparticles exposure had higher rate of respiratory support and excess length of hospital stay. Conclusion. Occupational COPD exacerbations are associated with chemical composition and mass concentration of nanoparticles in industrial aerosols
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Korkmaz, F. T., E. Symer, C. Odom, W. Molina, E. Na, L. Baird, Y. Kim, et al. "Expression of LOX-1 in the Lung Modulates Acute Pulmonary Inflammation During Pneumonia." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1221.
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Saperstein, SC, HL Huyck, CJ Johnston, JN Finkelstein, and GS Pryhuber. "Interleukin-1β Is Essential for Tumor Necrosis Factor-α-Induced Acute Pulmonary Inflammation in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1916.
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Chimenti, Laura, Raquel Guillamat, Neus Gomez, Jessica Tijero, LLuis Blanch, and Antonio Artigas. "Effects of nebulized heparin on pulmonary inflammation in a rat model of acute lung injury." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2138.
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Boe, Darren M., Tiffany R. Richens, Sarah A. Horstmann, William J. Janssen, Peter M. Henson, Marc Moss, and R. W. Vandivier. "Acute And Chronic Alcohol Exposure Impair The Clearance Of Apoptotic Cells And Enhance Pulmonary Inflammation." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1267.
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King, BA, and PS Kingma. "Surfactant Protein D Decreases Pulmonary Inflammation in Acute Respiratory Distress Syndrome Induced by Indirect Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3877.
Full textReports on the topic "Pulmonary acute inflammation"
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Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.
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Review question / Objective: This study is the protocol for a systematic review to evaluate the efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. we conducted a systematic review and meta-analysis of published randomized clinical trials (RCTs) of such combined therapy in the treatment of AECOPD, It provides a reliable scientific basis for clinicians to use this approach to treat AECOPD. Condition being studied: Chronic obstructive pulmonary disease is the third leading cause of death worldwide. AECOPD is the most common cause of hospitalization and death in patients with COPD. As lung function deteriorates and the disease progresses, the risk of alveolar hypoxia and consequent hypoxemia increases. Inflammation plays an important role in the progression of AECOPD. Modern medicine mainly treats AECPD by anti-inflammatory, relief of airway spasm, glucocorticoids, inhalants and other methods. Long-term application can easily lead to bacterial flora imbalance and drug resistance in patients. Comparatively, traditional Chinese medicine and acupuncture therapy are safe and effective.To assess the therapeutic efficacy and safety of HuaYu TongFu Method combined with acupuncture in AECOPD, we created a protocol for a systematic review to inform future clinical applications.