Дисертації з теми "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.
Повний текст джерелаKurti, 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.
Повний текст джерелаDepartment 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.
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.
Повний текст джерелаTiivistelmä 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
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.
Повний текст джерелаPetroni, 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/.
Повний текст джерелаSepsis 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
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.
Повний текст джерелаInterleukin-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. (...)
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.
Повний текст джерелаTo 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.
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.
Повний текст джерелаPneumonia 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
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/.
Повний текст джерелаBACKGROUND: 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.
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/.
Повний текст джерелаType 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.
Gaudet, Alexandre. "Biological role of endocan and of its major catabolite p14 in the regulation of acute lung inflammation : from physiopathology to prediction of ARDS." Thesis, Lille, 2018. http://www.theses.fr/2018LILUS059.
Повний текст джерелаARDS is defined as an acute diffuse, inflammatory lung injury associated with increased vascular permeability and leading to life-threatening respiratory failure. ARDS is still a severe and common condition in ICU patients, resulting from lung epithelial injuries (as observed in pneumonia) as well as systemic acute inflammatory states, such as septic shock, in which endothelial injury and excessive cellular recruitment play a major role. This condition is characterized by an increase in the migration of leukocytes and especially neutrophils from blood compartment into the lung. Following a firm adherence step depending on the interaction between the integrin LFA-1 and its endothelial ligand ICAM-1, transendothelial migration is based on complex molecular mechanisms involving on one hand endothelial adhesion molecules (E-selectine, ICAMs), and their leukocyte ligands (PSGL-1, LFA-1, Mac-1) and on the other hand chemotactic activators of leukocyte diapedesis (CXCL-12, CCL-2, IL-8) or inhibitors such as endocan.Endocan is a circulating proteoglycan mainly synthesized and secreted by lung endothelium. This molecule has been reported as a functional inhibitor of the LFA-1 / ICAM-1 interaction, explaining its ability to inhibit leukocyte recruitment. Consistently, low levels of endocan have been reported to be associated with high occurrence of respiratory failure in patients admitted in ICU with severe sepsis. This association could result from a lack of secretion of endocan leading to an insufficient protection against excessive lung inflammation in these patients. Another explanation could be advanced, based on the results from De Freitas Caires et al, who have reported the existence of a major catabolite of endocan produced under the proteolytic effect of neutrophil cathepsin G. This endocan fragment, named p14, devoid of the glycanic chain required for the anti-inflammatory activity of endocan, could be involved in the restoration of high levels of lung inflammation. Indeed, it could compete with endocan’s ability to interact with LFA-1, and then could reverse its biological anti-migratory effect. Thus, endocan and p14 could constitute an interesting innovative pathway integrating in much larger models that could finally improve the management of ARDS.During my PhD, we first investigated the effects of human endocan on transendothelial migration, then assessed the potential involvement of the LFA-1 / ICAM-1 interaction in those effects and finally evaluated the hypothetical anti-inflammatory effect of human endocan in a mouse LPS-induced ALI model. We also explored the effects of p14 on the endocan / LFA-1 / ICAM-1 interaction and its consequence on the recruitment of human leukocytes. Then, to assess whether those results concerning the effects of endocan and p14 in the field of basic science could be extrapolated for clinical investigations, we described the conditions of reliability of measurement of blood endocan in ICU patients. Finally, we aimed to comfort the prognostic value of blood endocan measured at ICU admission as a predictor of ARDS, thus supporting the hypothesis emitted by Palud et al, in an independent and larger cohort of patients
Barbosa, Susiane de Oliveira. "Efeito da suplementação com licopeno sobre o estresse oxidativo pulmonar induzido por lesão pulmonar aguda experimental." Universidade Estadual Paulista (UNESP), 2018. http://hdl.handle.net/11449/153467.
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A Síndrome do Desconforto Respiratório Agudo (SDRA) caracteriza-se por processo inflamatório que leva à quebra da barreira alvéolo-capilar com desenvolvimento de edema intersticial e alveolar, diminuição da complacência pulmonar, hipertensão pulmonar, desequilíbrio da relação ventilação/perfusão e hipoxemia refratária à administração de oxigênio. Apesar do progresso no entendimento de sua fisiopatologia e consequente avanço em estratégias terapêuticas de pacientes com SDRA, a mortalidade permanece elevada. Entre os mecanismos que levam a síndrome, várias evidências sugerem que pacientes portadores de SDRA estão expostos a elevado grau de estresse oxidativo (EO) induzido por ampla variedade de eventos. Por essa razão é fundamental a compreensão do papel do EO tanto na instalação como na perpetuação do processo infamatório que ocorre na doença. No entanto, apesar do uso de antioxidantes ter mostrado algum benefício na evolução da doença, ainda não há evidência clínica para sua utilização rotineira na prática. O licopeno é um carotenoide sem atividade provitamina A encontrado principalmente no tomate e nas frutas vermelhas. Em decorrência de seu grande número de duplas ligações conjugadas, o licopeno é considerado um dos melhores antioxidantes entre os carotenoides. Além disso, é um dos mais potentes antioxidantes encontrados no organismo humano, apresentando potência antioxidante 100 vezes maior do que a vitamina E e a vitamina C. A ventilação mecânica convencional protetora (VMC) constitui um dos principais pilares do tratamento da SDRA, sendo capaz de modificar a evolução da doença e reduzir a mortalidade. Baseado nos efeitos protetores da ventilação oscilatória de alta frequência (VOAF) sobre a SDRA, anteriormente descritos pelo grupo, bem como o potencial papel antioxidante e antiinflamatório do licopeno, nossa hipótese é que esse carotenoide exerce efeito protetor adicional em modelo experimental de SDRA. O objetivo do estudo foi investigar os efeitos da suplementação com licopeno sobre o EO pulmonar, por meio da capacidade antioxidante total (TAP) e dano oxidativo do DNA (teste do Cometa), em modelo experimental de lesão pulmonar induzida em coelhos ventilados com VMC e VOAF, comparando-os com grupo controle. Também foram avaliadas a histologia pulmonar e a inflamação pela contagem de células de neutrófilos no lavado broncoalveolar. Cinquenta e cinco coelhos foram instrumentados com traqueostomia, acessos vasculares e ventilados mecanicamente. Os animais suplementados receberam 10mg/Kg de licopeno durante 21 dias antes do experimento. A lesão pulmonar foi induzida por infusão traqueal de salina aquecida (30mL/Kg, 38°C). Foram formados os seguintes grupos experimentais: animais sadios foram submetidos a eutanásia para compor o grupo baseline sem suplementação: GBL; n=5 e baseline suplementado com licopeno: GBLL; n=5, animais sadios submetidos à VM Protetora, sem suplementação denominado grupo controle GC; n=5, animais submetidos à indução da lesão pulmonar e tratamento com ventilação mecânica e suplementados com licopeno GVMCL; n=10 e sem suplementação GVMC; n=10, com LP submetidos à VOAF e suplementados com licopeno GVAFL; n=10 e sem suplementação GVAF; n=10. Após a confirmação da lesão pulmonar, as gasometrias foram realizadas a cada 30 minutos pelas 4 horas de duração do protocolo experimental. O nível de significância foi de 5%. Comparando os momentos, antes e depois da lesão pulmonar em cada grupo, houve piora significante da oxigenação e também diminuição da complacência pulmonar estática em todos os grupos. Após 4 horas, os grupos tratados com VOAF, com e sem licopeno, e o grupo sob VMC protetora com licopeno, apresentaram melhora significante em relação ao grupo VMC protetora sem suplementação, apresentando relação de PaO2/FiO2 semelhante aos momentos antes da indução da lesão pulmonar e em relação ao GC. A contagem de neutrófilos no lavado broncoalveolar mostrou que os grupos GVMCL e GVAFL, apresentaram valores significantemente menores em comparação com os animais sem suplementação. GC, GVAFL e GVMCL apresentaram escore de lesão histológica significantemente menor quando comparados com os grupos sem suplementação. Quanto ao TAP no tecido pulmonar, não houve diferença estatística entre os grupos. O dano do DNA nos linfócitos, comparando os animais sob VMC protetora, foi significantemente mais baixo nos animais suplementados com licopeno. Este estudo demonstra que independentemente do modo ventilatório, a suplementação prévia com licopeno melhora a oxigenação, reduz a lesão inflamatória bem como a lesão histopatológica nos animais, assemelhando-se aos benefícios propostos pela VOAF, e minimiza o dano no DNA nos animais sob VMC protetora com suplementação em relação aos animais sob mesma ventilação.
Acute Respiratory Distress Syndrome (ARDS) is characterized by inflammatory process that leads to the breakdown of the alveolar-capillary barrier with the development of interstitial and alveolar edema, decreased pulmonary compliance, pulmonary hypertension, impaired ventilation and perfusion, and hypoxemia refractory to administration of oxygen. Despite better understanding in pathophysiology and consequent advancement in therapeutic strategies for ARDS patients, mortality remains high. Although the exact mechanism leading to ARDS is unknown, several evidences suggest that patients with the syndrome are exposed to a high degree of oxidative stress. For this reason it is important to understand the role of oxidative stress in both, initiation and progress of inflammatory process that occurs in the disease. However, although the use of antioxidants has shown some benefit in ARDS evolution, there is still no clinical evidence for its use in practice routine. Lycopene is a carotenoid with no provitamin A activity found mainly in tomatoes and red fruits. Due to its large number of double conjugated bonds, lycopene is considered one of the best antioxidants among carotenoids. In addition, it is one of the most potent antioxidants found in the human body, with antioxidant potency 100 times higher than vitamin E and vitamin C. Conventional mechanical ventilation (CMV) is the main ARDS treatment, capable of modifying disease evolution and reducing mortality. Based on the protective effects of high frequency oscillatory ventilation (HFOV) on ARDS, previously described by our group, as well as the potential antioxidant and antiinflammatory role of lycopene, our hypothesis is that this carotenoid has additional protective effect in ARDS model. The aim of this study was to investigate the effects of lycopene supplementation on pulmonary oxidative damage, analyzing total antioxidant performance (TAP) and oxidative DNA damage (Comet Assay), in an experimental induced lung injury model in rabbits, ventilated by CMV and HFOV compared to control group. Pulmonary histology and neutrophil cell counts were also evaluated. Fifty-five rabbits were instrumented with tracheostomy, vascular accesses and mechanically ventilated. Supplemented animals received 10mg/ kg of lycopene for 21 days prior to the experiment. Lung injury was induced by tracheal infusion of warm saline (30mL/ kg, 38°C). The following experimental groups were: healthy animals submitted to euthanasia to compose the baseline group without supplementation: GBL; n = 5 and baseline supplemented with lycopene: GBLL; n = 5, healthy animals submitted to Protective CMV, without supplementation, denominated GC control group; n = 5, animals submitted to lung injury induction and mechanical ventilation treatment and supplemented with lycopene GVMCL; n = 10 and without supplementation GVMC; n = 10, animals with LP submitted to HFOV and supplemented with lycopene GVAFL; n = 10 and without supplementation GVAF; n = 10. After confirming lung injury induction, blood gases were performed every 30 minutes during the 4 hours of the experimental protocol. The level of significance was 5%. Comparing the moments before and after the pulmonary injury induction in each group, there was a significant worsening of oxygenation and decrease in static lung compliance in all groups after injury induction. After 4 hours, groups treated with HFOV, with and without lycopene supplementation, and group with lycopene supplementation and submitted protective CMV, showed a significant improvement compared to Protective CMV group without supplementation, showing PaO2/FiO2 ratio similar to the moments before the pulmonary induction and CG. Neutrophil count in bronchoalveolar lavage showed that GVMCL and GVAFL groups presented significantly lower comparing with animals without supplementation. GC, GVAFL and GVMCL had a significantly lower histological injury score compared to groups without supplementation. TAP in lung tissue showed no statistical difference among groups. DNA damage on lymphocytes comparing animals submitted to protective CMV was significantly lower in animals supplemented with lycopene. This study demonstrates that independent of the ventilatory mode, prior lycopene supplementation improves oxygenation, reduced inflammatory injury, as well as histopathological injury score in this lung injury animal model. Both HFOV groups, and animals submitted to protective CMV and supplemented with lycopene showed reduced DNA-free damage compared to animals under de same ventilation without supplementation.
FAPESP: 2014/15683-9
Ribeiro, Alison. "Efeitos do canabidiol, um canabinóide derivado da Cannabis sativa, em um modelo murino de inflamação pulmonar aguda: uma avaliação imune-neuro-endocrinológica." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/10/10133/tde-01102012-162516/.
Повний текст джерелаCannabidiol (CBD), the major non-psychotropic plant (Cannabis sativa)-derived cannabinoid, is recognized for its immunossupressant and anti-inflammatory properties. Acute lung injury (ALI) is an inflammatory condition for which treatment is mainly supportive (ICU patients), because effective therapies have not been developed. Therefore, it was proposed an investigation in order to address the anti-inflammatory effects of CBD in a murine model of LPS-induced ALI, within an immune-neuro-endocrine perspective. To analyze the potential anti-inflammatory effect of CBD, it was evaluated total and differencial cell count of leukocytes present in the bronchoalveolar lavage (BAL) (migration of leukocytes into the lungs), myeloperoxidase activity in the lung tissue (indirect analysis of neutrophil activity), production of cytokines and chemokines in the BAL (analysis of the pulmonar inflammatory profile), protein (albumin) concentration in the BAL (indirect analysis of pulmonar vascular permeability), and expression of adhesion molecules (ICAM-1 and VLA-4) in leukocytes of the BAL. It was also analyzed the pharmacologic mechanism of the anti-inflammatory effects of CBD in the model of ALI, by using a highly selective antagonist of the adenosine A2A receptor (ZM241385). Finally, it was analyzed the neuro-endocrine effects of CBD in the context of lung inflammation; it was analyzed the general activity of the mice in the open field (analysis of sickness behavior) and the seric levels of corticosterone (activation of HPA (Hypothalamus-Hypophysis-Adrenal) axis). It was shown that both prophylactic (before the induction of inflammation) and therapeutic (after the induction of inflammation) protocols of treatment, with a sigle dose of CBD (20 or 80 mg/kg), has a long-term anti-inflammatory effect in mice submitted to the model of ALI (specially, after 1 and 2 days of the induction of inflammation). It was shown that CBD decreased leukocyte (neutrophil, macrophage, and lymphocytes) migration into the lungs, decreased cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2) in the BAL, decreased MPO activity in the lung tissue, decreased albumin concentration in the BAL, and decreased adhesion molecule expression (ICAM-1) in neutrophils of the BAL. It was also shown that adenosine A2A receptor is involved in the anti-inflammatory effects of CBD on LPS-induced ALI, because ZM241385 abrogated all of the anti-inflammatory effects of cannabidiol previously described. Finally, it was shown that CBD has discreet behavioral effects in the open field and was not able to activate the HPA axis. Thus, it was shown for the first time that both prophylactic and also therapeutic treatment with CBD (20 or 80 mg/kg) has a long-term anti-inflammatory effect in a murine model of ALI, most likely associated with an increase in the signaling through the adenosine A2A receptor. Hence, it is possible that in the future CBD may prove useful as a therapeutical tool in the treatment of pulmonar inflammatory conditions.
Costa, Natalia de Souza Xavier. "Efeito da exposição ao material particulado atmosférico no desenvolvimento da lesão pulmonar aguda (LPA) induzida por LPS." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-24112015-102031/.
Повний текст джерелаEpidemiological and experimental studies show that the air pollution can cause several harmful outcomes to the health, which include systemic and pulmonary inflammation, cardiovascular diseases, and exacerbation of preexisting diseases. The acute respiratory distress syndrome is characterized by intense inflammatory response, alveolo-capillary barrier damage and hypoxemia and since it was described for the first time in 1967 it still has high mortality rates. This study aims to 1. Evaluate the impact of urban air pollution exposure on the acute lung injury progression and 2. Evaluate if the LPS-induced injury is altered in an individual previously exposed to the air pollution. The main findings regarding objective 1 show that when there is an interaction of the particulate matter on the acute phase of LPS-induced injury, the lesion is not as severe as in the group that received only LPS. The inflammatory parameters show that inflammatory cells and pro inflammatory cytokines are increased in the LPS 24 hour, whereas not, or not as much as, in the air pollution + LPS group. Based on these results, we can hypothesize that may have occurred a shift of the inflammatory profile or immunotoxicity. Results of the objective 2 show that the group LPS + air pollution remains in a persistent inflammatory condition with increased leucocytes in BALF and pro inflammatory cytokines (IL-1beta, IL-6 e IL-8) also increased in the lung tissue, while the LPS 5 weeks group shows these parameters levels closer to the control group. The tissue morphology displays a diminished alveolar air space and septal thickening. It is very likely that the air pollution interferes on the adequate LPS-induced lesion recovery and repair, once that the air pollution, specially the fine particulate matter, has a continuous pro-inflammatory role over the lesion. We can conclude that: the use of nebulized LPS is a feasible acute lung injury model; the exposure to the particulate matter could alter the profile of the immediate response (24 hours) of the acute lung injury and it can impair the lesion recovery. Additional studies are necessary to understand the possible role of the immunological response modulation mechanisms involved in these processes
Holifanjaniaina, Sonia. "Rejet aigu en transplantation pulmonaire : intérêts de l’histologie et de l’ immunomarquage C4d dans le diagnostic de rejet aigu humoral et de l’évaluation de la polarisation des macrophages alvéolaires." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLV045/document.
Повний текст джерелаLung transplantation is considered as a valid therapeutic option for patients with end-stage lung disease. Despite considerable progress in immunosuppressive therapy, allograft rejection remains a major cause of graft loss. Multiple studies have highlighted the importance of acute rejection as an important risk factor for the development of chronic lung allograft dysfunction (CLAD) leading to graft failure. Therefore, the improvement in the diagnosis of acute rejection represents a major challenge to prevent CLAD. In this study, we evaluated the tissue markers of acute antibody-mediated rejection (AMR) in lung transplantation. In our experience, the histopathologic findings including the microvascular inflammation in pulmonary AMR are not specific and C4d staining is a useful marker to confirm the diagnosis of AMR. Secondly, we investigated by flow cytometry the polarization of alveolar macrophage obtained by bronchoalveolar lavage (BAL) from lung transplant patients with and without acute rejection. Our results show the limits of surface markers (CD206 and HLA-DR) in the evaluation of alveolar macrophage polarization. This study shows the interest of tissue markers, especially the C4d staining, in monitoring of lung transplant patients and highlights the need to identify appropriate and available markers for future studies of alveolar macrophage polarization by flow cytometry
"Aetiology and airway inflammation in acute exacerbations of chronic obstructive pulmonary disease." Thesis, 2007. http://library.cuhk.edu.hk/record=b6074809.
Повний текст джерелаChronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible.
Exhaled breath condensate (EBC) analysis is a novel tool which has been developed in recent years and the technique is believed to reflect the lower airway lining fluid. My previous work has demonstrated the repeatability of certain inflammatory markers in the EBC of stable asthma and COPD patients.
Hypothesis 1: Bacterial pathogens are the major cause of AECOPD with and without concomitant pneumonia in patients requiring hospitalization. In the one-year retrospective bacteriology study, there were 329 patients with 418 episodes of AECOPD without concomitant pneumonia. These result noted that H. influenzae was the commonest bacterium isolated in sputum in patients with AECOPD without concomitant pneumonia. In areas endemic of tuberculosis, it is advisable to use fluoroquinolones for AECOPD with caution in view of the positive sputum culture of mycobacterium tuberculosis in some patients.
Hypothesis 2: Viral pathogens are an important cause of AECOPD in patients hospitalized with AECOPD. For the prospective infectious aetiology study, there were 643 episodes of AECOPD among 373 patients (307 males). Severe airflow obstruction (stable state spirometry) was associated with a higher chance of positive sputum culture (28.2% for FEV1 ≥30% vs. 40.4% for FEV1 <30% predicted normal, p=0.006). In this study, Haemophilus influenzae and influenza A were the commonest aetiological agents in patients hospitalized with AECOPD. More severe airflow obstruction was associated with a higher chance of positive sputum culture.
Hypothesis 3: The rates of hospital admissions due to AECOPD are associated with indices of air pollution in Hong Kong. Concerning the effect of air pollutants on AECOPD, significant associations were found between hospital admissions for COPD with all 5 air pollutants. Adverse effects of ambient concentrations of air pollutants on hospitalization rates for COPD are evident, especially during the winter season in Hong Kong.
Hypothesis 4: During the course of AECOPD, it is possible to assess inflammation in the airway by measuring biomarkers non-invasively using the method of EBC collection. To explore the course of inflammation in the airway during AECOPD, 26 patients (22 male) with AECOPD (mean percentage predicted FEV1, 44.8 +/- 14.3), 11 stable COPD and 14 age and sex-matched healthy controls were studied. Repeatability measurements of TNFalpha and LTB4 in 6 stable COPD patients were satisfactory. EBC TNFalpha level was low in patients receiving systemic steroid and antibiotic therapy for AECOPD whereas EBC TNFalpha level was also lower in stable patients receiving ICS post AECOPD than those who were not. These findings suggest a potential role for serial EBC TNFalpha for non-invasive monitoring of disease activity.
Summary. The above studies have shown that bacterial pathogens are the major cause of AECOPD with and without concomitant pneumonia in patients requiring hospitalization and the commonest bacterium found in the sputum of the patients was Haemophilus influenzae. Viral pathogens are also an important cause of AECOPD in patients hospitalized with AECOPD in Hong Kong and the commonest virus identified in the NPA of the patients was influenza A. Concerning the effect of air pollutants on AECOPD, significant associations were found between hospital admissions for AECOPD with the air pollutants of SO2, NO3, O3, PM10 and PM2.5. Finally, TNFalpha could be measured in the EBC of patients during the course of AECOPD and its level was low in patients receiving systemic steroid and antibiotic therapy for AECOPD. The results suggest that it is possible to assess inflammation in the airway by measuring biomarkers non-invasively using the method of EBC collection. (Abstract shortened by UMI.)
Ko, Wai-san Fanny.
Source: Dissertation Abstracts International, Volume: 69-02, Section: B, page: 0926.
Thesis (M.D.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (leaves 207-250).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
School code: 1307.
Wulffen, Werner von [Verfasser]. "Role of lung dendritic cells in acute pulmonary inflammation / by Werner von Wulffen." 2008. http://d-nb.info/991921062/34.
Повний текст джерелаMielke, Carina Sybille [Verfasser]. "Netrin-1 dampens pulmonary inflammation during acute lung injury / vorgelegt von Carina Sybille Mielke." 2011. http://d-nb.info/1011230917/34.
Повний текст джерела"Lung inflammation associated with acute necrotizing pancreatitis in dogs and mice." Thesis, 2014. http://hdl.handle.net/10388/ETD-2014-05-1559.
Повний текст джерелаLee, Chou-hwei, and 李秋慧. "Autologous Transplantation of Endothelial Progenitor Cells Improves Pulmonary Gas Exchange and Reduces Alveolar Inflammation in Rabbits with Acute Lung Injury." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/19750122642258342442.
Повний текст джерела國立成功大學
細胞生物及解剖學研究所
97
Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are the most common causes of death in intensive care units and after major operation. The fundamental pathogenesis of ALI is increased alveolocapillary permeability largely due to inflammatory response in the pulmonary endothelium and alveoli. Activation and damage of pulmonary endothelium is another hallmark of ALI/ARDS. A number of endothelium-targeting therapies have been tested in clinical settings, but none of these restores pulmonary endothelial function during ALI/ARDS. Accumulating evidence suggests that peripheral blood contains bone marrow-derived progenitor cells. A portion of these circulating precursor cells can differentiate into mature endothelial cells and are referred to as endothelial progenitor cells (EPCs). Recent studies have demonstrated the therapeutic effects of EPCs on reendothelialization and neovascularization in patients with cardiovascular diseases. Previous report showed that autologous transplantation of EPCs attenuates pulmonary endothelial dysfunction and lung tissue damage in rabbits with oleic acid-induced ALI. Accordingly, this project examines the effect of EPCs on pulmonary reendothelialization in a more clinically relevant rabbit model of ALI induced by direct intratracheal instillation of lipopolysaccharide (LPS). Mononuclear cells were isolated from the peripheral blood of rabbits using the standard Ficoll gradient centrifugation. At day 7 of culture, the adherent cells, termed as early EPCs, were harvested for transplantation. Anesthetized rabbits received LPS (500 �慊/kg) via intratracheal instillation, and followed by autologous transplantation of EPCs through the ear vein. Rabbits were sacrificed 48 hours later and tissues were obtained for analysis. Compared with control, arterial oxygen content and saturation were higher in the EPC-treat animals, indicating that function of pulmonary alveolocapillary gas exchange was better preserved following transplantation of EPC. Endothelium-dependent relaxation response of pulmonary artery was significantly restored in rabbits received EPC transplantation. The degree of alveolar-capillary barrier leakage was measured by tissue Evans blue content, and was significantly reduced in EPC-treated group. Lung water content and degree of lung hemorrhage assessed by the lung wet-to-dry ratio and tissue hemoglobin were reduced in the EPC-treated group, respectively. Myeloperoxidase (MPO) activity was also reduced following transplantation of EPCs, indicating that activation and accumulation of neutrophils was attenuated in EPC-treated group. Collectively, our data underscore that autologous transplantation of EPCs attenuates LPS-induced ALI by restoring alveolocapillary and pulmonary endothelial function. Administration of EPCs can be a novel cell-based, pulmonary endothelium-targeted therapeutic strategy for ALI/ARDS.
Benediktus, Ewald [Verfasser]. "The role of T-cells in an acute and subchronic animal model of cigarette smoke-induced pulmonary inflammation = Die Rolle von T-Zellen in einem akuten und subchronischen Tiermodell der Zigarettenrauch-induzierten pulmonalen Entzündung / vorgelegt von Ewald Benediktus." 2010. http://d-nb.info/1008557854/34.
Повний текст джерелаChebli, Jasmine. "Le rôle des canaux potassiques dans la résolution des paramètres du syndrome de détresse respiratoire aiguë." Thèse, 2016. http://hdl.handle.net/1866/18897.
Повний текст джерелаAcute respiratory distress syndrome (ARDS) is characterized by alveolar-capillary barrier damage, resulting in the formation of pulmonary oedema and an exacerbated inflammatory response. Without rapid recovery of these parameters, there is a gradual development of fibrosis, leading to respiratory failure. It has been established that alveolar regeneration is a critical step for the resolution of ARDS. A better understanding of alveolar epithelial repair mechanisms is hence necessary to identify new therapies for ARDS, for which no effective treatment exist. It has been shown that repair mechanisms are regulated by membrane proteins, not only by growth factor receptors and integrins, but also by ion channels, in particular potassium channels. Therefore, the main objective of this study was to characterize the impact of KCa3.1 and KvLQT1 potassium channels modulation in the resolution of ARDS. First, our results have shown the cooperative role of the potassium channel KCa3.1, the extracellular matrix and the β1-integrin in alveolar epithelial repair processes in vitro. We have shown that the fibronectin matrix and KCa3.1 are involved in the migration and repair of primary cultures of rat alveolar cell monolayers. Our data also revealed a putative relationship between Kca3.1 and the β1-integrin. Second, we studied the impact of KvLQT1 potassium channel modulation on ARDS pathophysiological aspects with in vivo models. We showed that KvLQT1 was not only involved in alveolar epithelial repair, but also in the resolution of pulmonary oedema and inflammatory response. Taken together, our data demonstrate that potassium channels, such as KCa3.1 and KvLQT1, may be identified as potential therapeutic targets for the resolution of ARDS.