Relevant bibliographies by topics / Peripheral challenges and inflammation

Academic literature on the topic 'Peripheral challenges and inflammation'

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Published: 11 March 2023

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Journal articles on the topic "Peripheral challenges and inflammation"

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Ferrari, Carina C., and Rodolfo Tarelli. "Parkinson's Disease and Systemic Inflammation." Parkinson's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/436813.

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Peripheral inflammation triggers exacerbation in the central brain's ongoing damage in several neurodegenerative diseases. Systemic inflammatory stimulus induce a general response known as sickness behaviour, indicating that a peripheral stimulus can induce the synthesis of cytokines in the brain. In Parkinson's disease (PD), inflammation was mainly associated with microglia activation that can underlie the neurodegeneration of neurons in thesubstantia nigra(SN). Peripheral inflammation can transform the “primed” microglia into an “active” state, which can trigger stronger responses dealing with neurodegenerative processes. Numerous evidences show that systemic inflammatory processes exacerbate ongoing neurodegeneration in PD patient and animal models. Anti-inflammatory treatment in PD patients exerts a neuroprotective effect. In the present paper, we analyse the effect of peripheral infections in the etiology and progression in PD patients and animal models, suggesting that these peripheral immune challenges can exacerbate the symptoms in the disease.
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Blomqvist, Anders, and David Engblom. "Neural Mechanisms of Inflammation-Induced Fever." Neuroscientist 24, no. 4 (March 20, 2018): 381–99. http://dx.doi.org/10.1177/1073858418760481.

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Fever is a common symptom of infectious and inflammatory disease. It is well-established that prostaglandin E2 is the final mediator of fever, which by binding to its EP3 receptor subtype in the preoptic hypothalamus initiates thermogenesis. Here, we review the different hypotheses on how the presence of peripherally released pyrogenic substances can be signaled to the brain to elicit fever. We conclude that there is unequivocal evidence for a humoral signaling pathway by which proinflammatory cytokines, through their binding to receptors on brain endothelial cells, evoke fever by eliciting prostaglandin E2 synthesis in these cells. The evidence for a role for other signaling routes for fever, such as signaling via circumventricular organs and peripheral nerves, as well as transfer into the brain of peripherally synthesized prostaglandin E2 are yet far from conclusive. We also review the efferent limb of the pyrogenic pathways. We conclude that it is well established that prostaglandin E2 binding in the preoptic hypothalamus produces fever by disinhibition of presympathetic neurons in the brain stem, but there is yet little understanding of the mechanisms by which factors such as nutritional status and ambient temperature shape the response to the peripheral immune challenge.
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López-Ornelas, Adolfo, Adriana Jiménez, Gilberto Pérez-Sánchez, Citlali Ekaterina Rodríguez-Pérez, Alejandro Corzo-Cruz, Iván Velasco, and Enrique Estudillo. "The Impairment of Blood-Brain Barrier in Alzheimer’s Disease: Challenges and Opportunities with Stem Cells." International Journal of Molecular Sciences 23, no. 17 (September 4, 2022): 10136. http://dx.doi.org/10.3390/ijms231710136.

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Alzheimer’s disease (AD) is the most common neurodegenerative disorder and its prevalence is increasing. Nowadays, very few drugs effectively reduce AD symptoms and thus, a better understanding of its pathophysiology is vital to design new effective schemes. Presymptomatic neuronal damage caused by the accumulation of Amyloid β peptide and Tau protein abnormalities remains a challenge, despite recent efforts in drug development. Importantly, therapeutic targets, biomarkers, and diagnostic techniques have emerged to detect and treat AD. Of note, the compromised blood-brain barrier (BBB) and peripheral inflammation in AD are becoming more evident, being harmful factors that contribute to the development of the disease. Perspectives from different pre-clinical and clinical studies link peripheral inflammation with the onset and progression of AD. This review aims to analyze the main factors and the contribution of impaired BBB in AD development. Additionally, we describe the potential therapeutic strategies using stem cells for AD treatment.
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Vara, Sarina, Ioannis Kypraios, Ankur Thapar, Constantinos Kyriakides, and Shiva Dindyal. "Challenges in investigating Peripheral Vascular Disease in patients with Diabetes and Cardiovascular Diseases." International Journal of cardiodiabetes 1, no. 2 (October 1, 2022): 98–99. http://dx.doi.org/10.52964/ijcd.0015.

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Given the increasing prevalence of diabetes, with cardiovascular disease representing the principle cause of death and morbidity amongst diabetics, it is imperative that early investigation and then intervention is achieved. Diabetic patients are at increased risk of peripheral arterial disease (PAD), with an earlier onset and a more severe and diffuse manifestation often being seen. The key factors in diabetic arteriopathy include vascular smooth vessel dysfunction, inflammation, hypercoagulability and endothelial dysfunction. Moreover, the presence of PAD is a marker of generalised atherosclerosis and is a strong indicator of increased morbidity and mortality due to cardiovascular ischaemic events, with the risk of atherothrombotic events increasing in the presence of concomitant diabetes.
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Davis, Michael S., Chris M. Royer, Mark Payton, and Brian Buttress. "Modeling the acute- and late-phase responses to peripheral airway cooling and desiccation." Journal of Applied Physiology 93, no. 1 (July 1, 2002): 195–200. http://dx.doi.org/10.1152/japplphysiol.00074.2002.

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Acute bronchoconstriction after isocapnic hyperpnea can be produced in most asthmatic individuals. However, the existence of a late-phase response is less certain. We used a canine model of isocapnic hyperpnea to test the hypothesis that this discrepancy is due to differences in the challenge threshold for the responses. Acute-phase and late-phase bronchoconstriction was measured in nine dogs after peripheral airway exposure to unconditioned air. Additionally, bronchoalveolar lavage fluid (BALF) was obtained during the late-phase response. The acute-phase response was a polynomial function with a decreasing slope at higher challenges, whereas the late-phase response suggested that a minimum threshold of challenge severity was needed to produce late-phase bronchoconstriction. BALF leukocyte and eicosanoid concentrations had linear relationships with challenge severity. Our data support the hypothesis that acute- and late-phase posthyperpnea responses have different dose-response relationships, a fact that may explain the frequent lack of a late-phase response. However, our data suggest that mild inflammation can be induced with relatively lower challenge severity.
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Marottoli, Felecia M., Yuriko Katsumata, Kevin P. Koster, Riya Thomas, David W. Fardo, and Leon M. Tai. "Peripheral Inflammation, Apolipoprotein E4, and Amyloid-β Interact to Induce Cognitive and Cerebrovascular Dysfunction." ASN Neuro 9, no. 4 (July 14, 2017): 175909141771920. http://dx.doi.org/10.1177/1759091417719201.

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Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer’s disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. The goal of this study was to determine the interactive effect of APOE4, Aβ, and chronic repeated peripheral inflammation on cerebrovascular and cognitive dysfunction in vivo. EFAD mice are a well-characterized mouse model that express human APOE3 (E3FAD) or APOE4 (E4FAD) and overproduce human Aβ42 via expression of 5 Familial Alzheimer’s disease (5xFAD) mutations. Here, we utilized EFAD carriers [5xFAD+/−/ APOE+/+ (EFAD+)] and noncarriers [5xFAD−/−/ APOE+/+ (EFAD−)] to compare the effects of peripheral inflammation in the presence or absence of human Aβ overproduction. Low-level, chronic repeated peripheral inflammation was induced in EFAD mice via systemic administration of lipopolysaccharide (LPS; 0.5 mg/kg/wk i.p.) from 4 to 6 months of age. In E4FAD+ mice, peripheral inflammation caused cognitive deficits and lowered post-synaptic protein levels. Importantly, cerebrovascular deficits were observed in LPS-challenged E4FAD+ mice, including cerebrovascular leakiness, lower vessel coverage, and cerebral amyloid angiopathy-like Aβ deposition. Thus, APOE4, Aβ, and peripheral inflammation interact to induce cerebrovascular damage and cognitive deficits.
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Cloots, Roy H. E., Selvakumari Sankaranarayanan, Chiel C. de Theije, Matthew E. Poynter, Els Terwindt, Paul van Dijk, Theodorus B. M. Hakvoort, Wouter H. Lamers, and S. Eleonore Köhler. "Ablation of Arg1 in hematopoietic cells improves respiratory function of lung parenchyma, but not that of larger airways or inflammation in asthmatic mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 5 (September 1, 2013): L364—L376. http://dx.doi.org/10.1152/ajplung.00341.2012.

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Asthma is a chronic inflammatory disease of the small airways, with airway hyperresponsiveness (AHR) and inflammation as hallmarks. Recent studies suggest a role for arginase in asthma pathogenesis, possibly because arginine is the substrate for both arginase and NO synthase and because NO modulates bronchial tone and inflammation. Our objective was to investigate the importance of increased pulmonary arginase 1 expression on methacholine-induced AHR and lung inflammation in a mouse model of allergic asthma. Arginase 1 expression in the lung was ablated by crossing Arg1 fl/fl with Tie2Cre tg/− mice. Mice were sensitized and then challenged with ovalbumin. Lung function was measured with the Flexivent. Adaptive changes in gene expression, chemokine and cytokine secretion, and lung histology were quantified with quantitative PCR, ELISA, and immunohistochemistry. Arg1 deficiency did not affect the allergic response in lungs and large-airway resistance, but it improved peripheral lung function (tissue elastance and resistance) and attenuated adaptive increases in mRNA expression of arginine-catabolizing enzymes Arg2 and Nos2, arginine transporters Slc7a1 and Slc7a7, chemokines Ccl2 and Ccl11, cytokines Tnfa and Ifng, mucus-associated epithelial markers Clca3 and Muc5ac, and lung content of IL-13 and CCL11. However, expression of Il4, Il5, Il10, and Il13 mRNA; lung content of IL-4, IL-5, IL-10, TNF-α, and IFN-γ protein; and lung pathology were not affected. Correlation analysis showed that Arg1 ablation disturbed the coordinated pulmonary response to ovalbumin challenges, suggesting arginine (metabolite) dependence of this response. Arg1 ablation in the lung improved peripheral lung function and affected arginine metabolism but had little effect on airway inflammation.
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d’Alessandro, Elisa, Christian Becker, Wolfgang Bergmeier, Christoph Bode, Joshua H. Bourne, Helena Brown, Harry R. Buller, et al. "Thrombo-Inflammation in Cardiovascular Disease: An Expert Consensus Document from the Third Maastricht Consensus Conference on Thrombosis." Thrombosis and Haemostasis 120, no. 04 (April 2020): 538–64. http://dx.doi.org/10.1055/s-0040-1708035.

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AbstractThrombo-inflammation describes the complex interplay between blood coagulation and inflammation that plays a critical role in cardiovascular diseases. The third Maastricht Consensus Conference on Thrombosis assembled basic, translational, and clinical scientists to discuss the origin and potential consequences of thrombo-inflammation in the etiology, diagnostics, and management of patients with cardiovascular disease, including myocardial infarction, stroke, and peripheral artery disease. This article presents a state-of-the-art reflection of expert opinions and consensus recommendations regarding the following topics: (1) challenges of the endothelial cell barrier; (2) circulating cells and thrombo-inflammation, focused on platelets, neutrophils, and neutrophil extracellular traps; (3) procoagulant mechanisms; (4) arterial vascular changes in atherogenesis; attenuating atherosclerosis and ischemia/reperfusion injury; (5) management of patients with arterial vascular disease; and (6) pathogenesis of venous thrombosis and late consequences of venous thromboembolism.
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Tebbutt, Scott J., Jian-Qing He, Amrit Singh, Casey P. Shannon, Jian Ruan, and Chris Carlsten. "Transcriptional Changes of Blood Eosinophils after Methacholine Inhalation Challenge in Asthmatics." Genomics Insights 5 (January 2012): GEI.S9125. http://dx.doi.org/10.4137/gei.s9125.

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Background Methacholine challenge is commonly used within the asthma diagnostic algorithm. Methacholine challenge has recently been shown to induce airway remodelling in asthma via bronchoconstriction, without additional airway inflammation. We evaluated the effect of methacholine-induced bronchoconstriction on the peripheral whole-blood transcriptome. Methods Fourteen males with adult-onset, occupational asthma, 26–77 years of age, underwent methacholine inhalation challenges. The concentration of methacholine eliciting a ≥20% fall in FEV1 (PC20) was determined. Blood was collected immediately prior to and two hours after challenge. Complete blood counts and leukocyte differentials were obtained. Transcriptome analysis was performed using Affymetrix GeneChip® Human Gene 1.0 ST arrays. Data were analyzed using robust LEMMA and SAM. The cell-specific Significance Analysis of Microarrays (csSAM) algorithm was used to deconvolute the gene expression data according to cell type. Results Microarray pathway analysis indicated that inflammatory processes were differentially affected. CsSAM identified 1,559 transcripts differentially expressed (all down-regulated) between pre- and post-methacholine in eosinophils at a false discovery cutoff of 10%. Notable changes included the GOLGA5 and METTL2B genes and the protein ubiquitination and CCR3 pathways. Conclusions We demonstrated significant changes in the peripheral blood eosinophil-specific transcriptome of asthmatics two hours after methacholine challenge. CCR3 and protein ubiquitination pathways are both significantly down-regulated.
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Levy, Ryan M., Jose M. Prince, Runkuan Yang, Kevin P. Mollen, Hong Liao, Gregory A. Watson, Mitchell P. Fink, Yoram Vodovotz, and Timothy R. Billiar. "Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (October 2006): R970—R976. http://dx.doi.org/10.1152/ajpregu.00793.2005.

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Extensive soft tissue injury and bone fracture are significant contributors to the initial systemic inflammatory response in multiply injured patients. Systemic inflammation can lead to organ dysfunction remote from the site of traumatic injury. The mechanisms underlying the recognition of peripheral injury and the subsequent activation of the immune response are unknown. Toll-like receptors (TLRs) recognize microbial products but also may recognize danger signals released from damaged tissues. Here we report that peripheral tissue trauma initiates systemic inflammation and remote organ dysfunction. Moreover, this systemic response to a sterile local injury requires toll-like receptor 4 (TLR4). Compared with wild-type (C3H/HeOuJ) mice, TLR4 mutant (C3H/HeJ) mice demonstrated reduced systemic and hepatic inflammatory responses to bilateral femur fracture. Trauma-induced nuclear factor (NF)-κB activation in the liver required functional TLR4 signaling. CD14−/− mice failed to demonstrate protection from fracture-induced systemic inflammation and hepatocellular injury. Therefore, our results also argue against a contribution of intestine-derived LPS to this process. These findings identify a critical role for TLR4 in the rapid recognition and response pathway to severe traumatic injury. Application of these findings in an evolutionary context suggests that multicellular organisms have evolved to use the same pattern recognition receptor for surviving traumatic and infectious challenges.
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Dissertations / Theses on the topic "Peripheral challenges and inflammation"

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Chapman, Katie. "Peripheral inflammation after experimental stroke." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518434.

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McColl, Alison. "The brain response to peripheral inflammation." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6764/.

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Communication between the immune system and the central nervous system (CNS) is becoming increasingly topical as evidence suggests the two systems are intricately linked. Although the brain is considered an ‘immune-specialised’ tissue, it is not free from the influences of the periphery. Recent data indicate that peripheral immune stimulation can significantly affect the CNS, and patients with chronic inflammatory diseases, including rheumatoid arthritis (RA) and psoriasis, are often further burdened by the onset of neuropsychiatric conditions such as major depressive disorder (MDD), schizophrenia and anxiety. However, despite increases in our understanding, the precise mechanisms underpinning this relationship remain unclear. Therefore, the aim of this thesis is to investigate the communication pathways that exist between the immune system and the nervous system and to enhance our understanding of this bidirectional relationship. Using a well-characterised animal model of psoriasis-like skin inflammation, I have investigated the effects of cutaneous, peripheral inflammation on the brain. Psoriasis-like skin inflammation was induced in female C57BL/6 mice via the repeated application of Aldara cream to the shaved dorsal skin. Twenty-four hours after the fifth application, the transcriptional response in the brain was assessed and compared with mice treated with an aqueous control cream, using Affymetrix GeneChip arrays. The induction of target genes, identified using microarray analysis, was confirmed in an independent model using QPCR and was compared to the gene induction following a number of other inflammatory models, including a sterile model of cutaneous inflammation. Transcriptional profiling techniques allowed me to identify a number of differentially expressed genes in the brains of Aldara- and Imiquimod (IMQ)- treated mice when compared with the brains of control mice. This response included a range of interferon-stimulated genes (ISGs) and chemokines that were not induced in the peripheral blood leukocytes (PBL), and occurred independently of an overt cytokine response in the PBL. The brain ISG and chemokine response was not detected following a sterile model of cutaneous inflammation or following the intraperitoneal administration of Imiquimod.  The central induction of a number of chemokines prompted the evaluation of immune cell infiltration into the brain parenchyma. In addition, the functional consequences of topical Aldara treatment, and the involvement of inflammatory chemokines, were determined by assessing dentate neurogenesis and burrowing behaviour in wild-type and ACKR2-deficient mice. The transcriptional response following cutaneous IMQ-induced inflammation is indicative of a peripherally triggered inflammatory response in the brain. In addition, the data described in this thesis demonstrate a functional consequence of peripheral immune stimulation and suggest that cutaneous inflammation could modulate the recruitment of leukocytes to the brain. These data highlight a potential mechanism of TLR-dependent communication between the periphery and the brain that could be mediated through the activation of the afferent vagus nerve.
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Adeoye, Opeolu M. D. "Peripheral Leukocytes and Intracerebral Hemorrhage." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1353100438.

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Jiang, Yanyan. "The role of peripheral TNF in acute brain inflammation." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.496980.

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Gherhes, Cristian. "The challenges of entrepreneurship in peripheral post-industrial places." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/20317/.

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The UK has a long history of spatial disparity in economic prosperity across its regions which, despite periodic shifts in its geographies of economic development governance, have persisted. As such, a key question that continues to preoccupy economic geographers is why some local and regional economies are more capable of renewal and transformation than others which remain locked in decline or underperformance. Research has hitherto highlighted the importance of ‘place’ and institutional context in shaping the outcomes of economic development. At the same time, the role of entrepreneurship as an engine of economic development is widely acknowledged, yet there is significant heterogeneity in the nature and level of entrepreneurial activity across places, with previous research highlighting the key role of institutions in shaping its outcomes. The thesis addresses these debates through a focus on entrepreneurship in peripheral post-industrial places (PPIPs), with the aim of examining the institutional challenges to fostering more entrepreneurial and resilient PPIPs.
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Barr, Laura Caroline. "Peripheral blood mononuclear cell depletion for experimental human lung inflammation." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/23705.

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Acute lung injury (ALI) affects a significant proportion of patients requiring critical care and is associated with high morbidity and mortality. Treatment is currently only supportive, with no pharmacological treatment yet shown to definitively improve outcome. There is evidence from murine models of ALI that monocytes play a key role in the development of the neutrophilic lung infiltration characteristic of ALI. Depletion of blood monocytes in mice given intra-tracheal lipopolysaccharide (LPS) significantly reduces pulmonary neutrophil influx, systemic neutrophilia and other markers of lung injury. In humans, monocyte-like cells have been documented in the bronchoalveolar lavage (BAL) fluid of patients with a variety of inflammatory lung conditions, including ALI. This thesis describes novel work performed in healthy human subjects to test whether, in an experimental model of human lung inflammation, depletion of circulating blood monocytes can ameliorate systemic and pulmonary inflammation. LPS inhalation is an established method of modelling ALI in healthy human subjects as it safely and consistently induces mild and self-limiting systemic and pulmonary inflammation. A preliminary study in a group of 12 healthy subjects confirmed the safety and efficacy of LPS inhalation compared to saline placebo. LPS inhalation induced a marked blood neutrophilia together with a rise in body temperature and heart rate and elevated BAL neutrophil and pro-inflammatory cytokine concentrations. This study also used flow cytometry to confirm the presence of pulmonary monocyte-like cells (PMLCs) in BAL fluid, which, although distinct from blood monocytes, could be clearly divided into two separate sub-types according to CD14/CD16 expression. LPS inhalation caused a rise in the number of circulating classical monocytes in blood and an expansion in the CD14++CD16- 'inducible' iPMLC subtype (reminiscent of classical blood monocytes), compared to the CD14++CD16+ 'resident' rPMLC subtype. This may represent transmigration of classical monocytes from blood across the pulmonary endothelium. In humans, mononuclear cell (MNC) leukapheresis provides a readily available method of depleting circulating blood monocytes. A second preliminary study, performed in a separate group of 6 healthy subjects, demonstrated that leukapheresis of four total blood volumes could be safely employed to deplete large numbers of circulating blood monocytes. Active recruitment of monocytes into circulating blood during leukapheresis did, however, limit the reduction in total circulating blood monocyte counts. This study also investigated, for the first time, the potential pulmonary effects of leukapheresis. Despite a relative prominence of iPMLCs in BAL fluid after leukapheresis, there was no evidence of significant neutrophil influx or a clinically important pro-inflammatory effect in the alveolar space. A randomised, double blind, placebo-controlled trial was then performed in a third group of 30 healthy human subjects who all inhaled LPS at baseline. There was no evidence that MNC leukapheresis (depletion group, n=15), compared to a sham procedure (sham group, n=15), attenuated the systemic and pulmonary inflammation induced by LPS inhalation, as measured by: blood neutrophil and plasma C-reactive protein (CRP) levels; by the neutrophil, protein and pro-inflammatory cytokine content of BAL fluid; and by [18F]fluorodeoxyglucose positron emission tomography ([18F]FDG PET)-derived measures of global lung inflammation. MNC leukapheresis temporarily prevented the LPS-induced rise in circulating classical monocytes and was also associated with a small reduction in the estimated numbers of MNCs in BAL fluid. It did not, however, appear to affect the LPS-induced expansion in the iPMLC subtype. Further characterisation of the PMLC subtypes by flow cytometry/sorting and cell culture demonstrated that the iPMLC subtype was more pro-inflammatory but less mature and with a lower proliferation potential than the rPMLC subtype. In summary, this work did not support a role for circulating blood monocytes in the evolution of LPS-induced systemic or pulmonary neutrophilia in man. The rise in circulating levels of classical blood monocytes and the dramatic expansion of pro-inflammatory, immature iPMLCs in BAL fluid after LPS inhalation do, however, suggest that monocytes migrate to the lung and are to some extent involved in the pathogenesis of lung inflammation. Compared to murine methods of monocyte depletion, leukapheresis could not achieve such an extensive or sustained reduction in circulating blood monocyte counts, nor was it likely to have influenced other (specifically patrolling or splenic) monocyte pools. Future work in the drive to find treatments for ALI should therefore investigate the potential of pre-emptive leukapheresis or the efficacy and safety of other methods of human monocyte depletion in experimental lung inflammation.
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Karim, Salman. "Peripheral and central markers of inflammation in mild cognitive impairment." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/peripheral-and-central-markers-of-inflammation-in-mild-cognitive-impairment(bd21dafe-65c1-42c9-949b-733abfc71037).html.

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There has been accumulating scientific evidence, over the last three decades, of the role of inflammatory processes in the development of Alzheimer's disease (AD). Population based studies suggest that plasma levels of inflammatory markers are raised in peripheral blood of people with AD. People on long term use of non-steroidal anti-inflammatory drugs have a lower prevalence of AD. Moreover, both animal and human histopathology studies have reported localization of inflammation in brain areas primarily affected by AD pathology. Areas of increased inflammation can be visualized in vivo by Positron Emission Tomography (PET) scans using the PK11195 ligand that binds with the benzodiazepine receptor sites of activated microglial cells. Cognitive decline in AD has been shown to correlate with levels of microglial activation using PK11195 PET scans. People with amnestic mild cognitive impairment (MCI) are known to be at high risk of developing AD.We aimed to investigate the association between peripheral and central markers of inflammation and cognitive decline in a group of people with amnestic MCI.MCI subjects (n=70) underwent cognitive testing, IL-6 and CRP in peripheral blood were measured and repeated after 1 year. A sub group (n=15) was followed up for another year and central brain microglial activation was measured by PET using PK11195 along with cognitive and peripheral inflammatory marker measurement. The mean CRP and IL-6 levels of the cohort increased over one year but the rise was only significant for CRP. No association was detected between inflammatory markers levels and cognition as measured by a battery of cognitive instruments. Group comparisons of the PET cohort with healthy controls (n=5) showed increased PK11195 binding (mean binding potential) in frontal lobe, temporal lobe, parietal lobe, putamen, occipital lobes and significantly increased binding in posterior cingulate gyrus. This study, to our knowledge, is unique in studying makers of inflammation in amnestic MCI participants both in peripheral blood and brain. The results of this study, in the light of current literature, add to the importance of recognition of inflammatory processes in people at risk of developing AD. The results suggest that CRP levels rise significantly over time and are detectable in peripheral blood by using practically simple laboratory techniques. The results also suggest that activated microglia in amnestic MCI patients can be visualized in vivo by using PK11195 PET scans and show higher levels of activation as compared to healthy controls. These finding could be useful in identifying people with malactivated (pro-inflammatory) microglia as potential targets for prevention/early treatment strategies. Further studies with larger samples sizes and long term follow-up are needed to investigate whether these peripheral and central inflammatory markers could shed light on the aetiology of AD and be useful in monitoring disease progression.
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Thomson, Carolyn. "Peripheral inflammation remotely triggers global gene expression changes in the brain." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5390/.

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Although the central nervous system (CNS) was once considered an immunologically privileged site, in recent years it has become increasingly evident that cross talk between the immune system and the CNS does occur. As a result, patients with chronic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease or psoriasis are often further burdened with neuropsychiatric symptoms such as depression, anxiety and fatigue. Despite the recent advances in our understanding of neuroimmune communication pathways, the precise effect peripheral immune activation has on neural circuitry remains unclear. Therefore, the primary aim of this thesis was to develop a better understanding of the bidirectional relationship, and communication pathways, that exist between the immune system and the nervous system. By utilising transcriptomics in a well-characterised murine model of systemic inflammation, I have investigated the molecular mechanisms by which inflammation originating in the periphery can induce transcriptional modulation in the brain. Systemic inflammation was induced in male C57BL/6 mice via intraperitoneal injection of lipopolysaccharide (LPS). After 48 hours, whole brain transcriptional profiles were assessed, and compared to that of a vehicle- treated control group, using Affymetrix GeneChip microarrays. Target gene induction, identified by microarray analysis was validated independently using QPCR. Expression of the same panel of target genes was then investigated, in the brains of mice, following the induction of different sterile, and TLR- dependent, models of peripheral inflammation. Microarray analysis of whole brains collected 48hr after LPS challenge revealed increased transcription of a range of interferon-stimulated genes (ISGs) in the brain, including a significant upregulation of the classic interferon-induced chemokine CXCL10. This transcriptional profile could not be reproduced by the systemic administration of TNFα, or following lipoteichoic acid-induced systemic inflammation. However, target genes remained induced in the brain following daily LPS injections, in the absence of a detectable inflammatory cytokine response in the periphery. 1 The central induction of CXCL10 suggests that acute exposure to LPS in the periphery may prime the brain for T cell infiltration. This prompted an investigation into whether leukocytes infiltrated the brain following daily systemic LPS injections. First, the inflammatory chemokine repertoire in the brains of LPS treated mice was systematically characterised. In addition to Cxcl10, repeated injection of LPS in the periphery triggered a transient increase in the transcription of a number of other inflammatory chemokines in the brain. Chemokine induction was associated with an influx of leukocytes from the periphery, and an increase in mRNA encoding the relevant chemokine receptors. Therefore, chemokine induction in the brain following daily systemic LPS injections may mediate the recruitment of leukocytes from the periphery. The transcriptional response in the brain following systemic LPS challenge is indicative of a peripherally triggered inflammatory response in the brain. The data described in this thesis highlight a potential mechanism of gene modulation in the brain which may be dependent on a TLR-induced type I interferon response. Considerable evidence links type I interferons to psychiatric disorders, and consequently, interferon production in the brain could represent an important mechanism linking peripheral TLR-induced inflammation with behavioural changes. In addition, the data described in this thesis demonstrate that chronic exposure to LPS in the periphery may remotely modulate the recruitment of leukocytes to the brain. This highlights a potential protective mechanism that could prevent a chronic bacterial infection from spreading from the periphery to the brain.
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Tzoulaki, Ioanna. "Inflammation and haemostasis in the development and progression of peripheral atherosclerotic disease." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/2148.

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Peripheral arterial disease (PAD) defines atherosclerotic disease of the arteries to the legs. PAD begins early in life and remains asymptomatic over long periods. The ankle brachial index (ABI) is an important diagnostic test which can identify asymptomatic individuals and serve as a good marker of the underlying peripheral and systemic atherosclerosis. Recent advances in vascular biology proposed a role of inflammatory and haemostatic mechanisms in atherosclerotic disease. Although inflammatory and haemostatic markers have been associated with coronary atherosclerosis in large scale epidemiological studies their role in PAD development is not well established and for many markers unknown. Also, their relationship with the progression of early asymptomatic disease has not been studied before. The aim of this thesis was to examine 12 markers of inflammation and haemostasis in relation to peripheral atherosclerotic progression and incident PAD. The Edinburgh Artery Study was used for this analysis. This is a population based cohort study of 1,592 men and women recruited in 1987. ABI was measured at baseline and at two follow up examinations which were conducted after 5 and after 12 years. Also, subjects were followed up for cardiovascular events for 17 years. Conventional cardiovascular risk factors, C-reactive protein (CRP), interleukin-6 (IL-6), intercellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin, fibrinogen, D-dimer, tissue plasminogen activator (t-PA), vonWillebrand factor (vWF), factor VII, fibrinopeptide A (FpA) and prothrombin fragments 1+2 (F1+2) were measured at baseline. Valid ABI measurements were available for 1,582 subjects at baseline, for 1,081 subjects at the 5 year follow up and for 816 subjects at the 12 year follow up. The population showed a progression in atherosclerotic disease assessed by the mean ABI decline over time. The mean change in ABI was -0.04 (0.18) after 5 years and -0.06 (0.19) after 12 years. From inflammatory markers, CRP (p <0.01), IL-6 (p <0.001) and ICAM-1 (p <0.01) were associated with atherosclerotic progression after 12 years, independently of baseline ABI and of conventional cardiovascular risk factors. Also, from haemostatic markers, fibrinogen (p =0.05) and D-dimer (p ≤ 0.05) were significantly associated with atherosclerotic progression independently of baseline ABI and cardiovascular risk factors. Moreover, subjects with higher levels of both D-dimer and IL-6 at baseline had the greatest ABI decline. Also, IL-6 showed the stronger independent effect on atherosclerotic progression and retained statistical significance after adjustments for all inflammatory markers and for fibrinogen and D-dimer. Approximately 26% of the baseline population developed at least one event of major CVD and 14% of the baseline population developed symptomatic PAD after 17 years of follow up. Inflammatory markers, CRP and IL-6 showed modest associations with PAD which lost statistical significance in the multivariable model. On the other hand, these markers were associated with incident major CVD with hazard ratios (95% CI) 1.6 (1.2, 2.3) and 1.8 (1.3, 2.6) respectively (top vs. bottom tertile) in the multivariable model. ICAM-1 showed weak associations with incident CVD, however, was significantly associated with PAD with hazard ratio (95% CI) 1.8 (1.2, 2.7) (top vs. bottom tertile) after adjustments for cardiovascular risk factors and CVD at baseline. Haemostatic markers, fibrinogen and D-dimer were associated with 2.2 (95% CI: 1.5, 3.2) and 1.7 (1.2, 2.6) increase in the risk of PAD development and 1.8 (1.3, 2.3) and 1.6 (1.2, 2.1) increase in the risk of CVD independently of cardiovascular risk factors and history of CVD at baseline, respectively. This analysis showed a major role of inflammatory markers, CRP, IL-6 and ICAM-1 in atherosclerotic development and progression. In addition, fibrinogen and D-dimer, but not other haemostatic factors, were associated with progressive and incident peripheral atherosclerosis. Since D-dimer and fibrinogen are acute phase reactants, these data support the hypothesis that inflammation is more related to atherosclerosis than is hypercoagulation. Most importantly, the majority of the reported associations were not explained by increased levels of cardiovascular risk factors or pre-existing clinical or subclinical arterial disease. Thus these markers are more likely to have a causal than a consequential role in atherosclerotic disease.
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Parmar, Jiteshkumar H. "The role of inflammation in ischaemia reperfusion injury due to peripheral arterial revascularisation." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509840.

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Books on the topic "Peripheral challenges and inflammation"

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Schäfer, Michael, and Christoph Stein, eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS. Basel: Birkhäuser Basel, 2003. http://dx.doi.org/10.1007/978-3-0348-8039-8.

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Ilonszki, Gabriella, and Christophe Roux, eds. Opportunities and Challenges for New and Peripheral Political Science Communities. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-79054-7.

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Davis, Terry Edward, ed. Peripheral visions: Politics, society, and the challenges of modernity in Yucatan. Tuscaloosa: University of Alabama Press, 2010.

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Peripheral visions: Politics, society, and the challenges of modernity in Yucatan. Tuscaloosa: University of Alabama Press, 2010.

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Falk Symposium (76th 1994 Estoril, Portugal). Inflammatory bowel diseases: New insights into mechanisms of inflammation and challenges in diagnosis and treatment. Dordrecht: Kluwer Academic Publishers, 1995.

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De Leo, Joyce A., 1960-, Sorkin Linda S. 1953-, Watkins Linda R. 1954-, and International Association for the Study of Pain., eds. Immune and glial regulation of pain. Seattle: IASP Press, 2007.

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Fatima Shad, Kaneez, ed. Erythrocyte - A Peripheral Biomarker For Infection and Inflammation. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.92510.

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Shad, Kaneez Fatima. Erythrocyte: A Peripheral Biomarker for Infection and Inflammation. IntechOpen, 2021.

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(Editor), Michael Schäfer, and Christoph Stein (Editor), eds. Mind over Matter - Regulation of Peripheral Inflammation by the CNS (Progress in Inflammation Research). Birkhäuser Basel, 2004.

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Baldelomar, Raquel, and Richard Jacoby. Sugar Crush: How to Reduce Inflammation, Reverse Nerve Damage, and Reclaim Good Health. HarperCollins Publishers, 2015.

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Book chapters on the topic "Peripheral challenges and inflammation"

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Perrotte, Morgane, Joel Pincemail, Mohammed Haddad, and Charles Ramassamy. "Redox Based-Peripheral Biomarkers in Alzheimer’s Disease: Challenges, Limits and Prospects." In Inflammation, Aging, and Oxidative Stress, 377–97. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33486-8_19.

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Olszewski, Waldemar L., and Marzanna T. Zaleska. "Inflammation." In Peripheral Lymphedema, 119–30. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3484-0_15.

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Gupta, Noopur, Yogita Gupta, M. Vanathi, and Radhika Tandon. "Peripheral Ulcerative Keratitis." In Corneal Infection and Inflammation, 92–109. First edition. | Boca Raton, FL : CRC Press, 2021.: CRC Press, 2021. http://dx.doi.org/10.1201/9781003024897-10.

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Lim, Alvin, Katarina Krajina, and Anna L. Marsland. "Peripheral Inflammation and Cognitive Aging." In Inflammation in Psychiatry, 175–87. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000346362.

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Murta, Verónica, and Carina Ferrari. "Peripheral Inflammation and Demyelinating Diseases." In Advances in Experimental Medicine and Biology, 263–85. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-40764-7_13.

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Lever, Isobel. "Inflammation, Modulation by Peripheral Cannabinoid Receptors." In Encyclopedia of Pain, 1612–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_1943.

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Carlton, Susan M. "Inflammation, Role of Peripheral Glutamate Receptors." In Encyclopedia of Pain, 1615–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_1945.

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Shaikh, Sikandar. "PET-CT in Peripheral Vascular Pathologies." In PET-CT in Infection and Inflammation, 131–41. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-9801-2_9.

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Griffith, James F., and Roman Guggenberger. "Peripheral Nerve Imaging." In IDKD Springer Series, 259–68. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71281-5_18.

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AbstractThis chapter reviews the basics and practicalities of imaging the peripheral nerves with ultrasound and MRI. Nerve entrapment, tumours, trauma, and inflammation are covered. The complimentary role of ultrasound and MRI in imaging peripheral nerve disorders is stressed.
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Kamer, Angela R., Ronald G. Craig, and Mony J. de Leon. "Peripheral Inflammation and Alzheimer’s Disease: Periodontal Disease." In A Clinician's Guide to Systemic Effects of Periodontal Diseases, 93–106. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49699-2_8.

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Conference papers on the topic "Peripheral challenges and inflammation"

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Dalli, Jesmond, Ana Rodriguez, Bernd Spur, and Charles Serhan. "Structure elucidation and biological evaluations of sulfido-conjugated specialized pro-resolving mediators." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/mqgv6628.

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Inflammatory diseases are characterized by unabated inflammation that leads tissue destruction resulting in malaise. Whilst much is known on the mechanism that perpetuate inflammation, less is known about the molecules and pathways that coordinate the termination of inflammation and facilitate the repair and regeneration of damaged tissues. To evaluate the potential contribution of essential fatty acid-derived mediators in coordinating this life saving response we interrogated inflammatory exudates obtained following self-limited inflammatory challenge. Using radio-isotope tracking we found that the omega-3 fatty acid docosahexaenoic acid is utilized to produce novel bioactive molecules in these exudates. The structures of these molecules were elucidated using a range of physical techniques, demonstrating that these molecules were peptide lipid conjugated mediators and the stereochemistry of the functional groups was established using total organic synthesis. Investigations into their biosynthetic pathways demonstrated that the formation of their formation was initiated via the 14-lipoxygenation of DHA, that was then converted into an intermediate allylic epoxide and then conjugated to glutathione to yield the first mediator in the family which was coined as maresin conjugated in tissue regeneration (MCTR)1. This was then further converted to to 13-cysteinylglycinyl,14-hydroxy-docosahexaenoic acid (MCTR2) and 13-glycinyl,14-hydroxy-docosahexaenoic acid (MCTR3). Evaluation of the biological activities of these molecules demonstrated that they limited the recruitment of inflammatory cells to the sites of both sterile and infectious challenge. They reprogrammed biology towards a tissue protective phenotype and promoted the repair and regeneration of damaged tissues. Evaluation of the levels of these mediators in human peripheral blood demonstrated that the production of MCTR3 is significantly reduced in patients with rheumatoid arthritis that display signs of erosive joint disease. Together, these findings identify previously undescribed chemical signals that enhance host responses to limit inflammation, stimulate resolution of inflammation, and promote the restoration of function.
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Machado, Luiza, Camila Santos, Bianca Leonardi, Andréia Rocha, Igor Fontana, Bruna Bellaver, Gianina Venturin, et al. "ACUTE PERIPHERAL INFLAMMATION IMPACT ON CEREBRAL GLUCOSE METABOLISM." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda072.

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Background: Neuroinflammation is a phenomenon already described in Alzheimer’s disease (AD). However, the effect of peripheral inflammation in AD is less understood. We recently demonstrated that severe sepsis causes acute brain metabolic disturbances. Nevertheless, whether mild acute peripheral inflammation affects brain metabolism remains unclear. Objective: We aimed at investigating the impact of mild acute peritonitis on glucose brain metabolism. Methods: Adult male wistar rats (n=6, per group) received a single intraperitoneal injection of 500 ml of carrageenan (CG, 500 µg of carrageenan i.p.) or saline (CO). Brain glucose metabolism was assessed using (18F) FDG-PET 4h after i.p. injections, which represents the first peak of inflammation. The peripheral inflammatory process was evaluated by analyzing the peritoneal lavage in a flow cytometer 48h after the injections, during the second peak of inflammation. Results: The CG animals presented a 5-fold increase in macrophages numbers (p0,05). However, carrageenan-induced inflammation did not cause acute changes in brain glucose metabolism (p>0,05). Conclusion: Mild acute peripheral inflammation does not change brain glucose metabolism. Further evaluations aiming to investigate long-term consequences of sustained mild inflammation are needed.
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Takeyama, K., A. Kurokawa, T. Akaba, K. Arimura, S. Muramatsu, K. Isono, M. Kondo, and E. Tagaya. "Mucus Accumulation in Peripheral Airways: Comparison Between Neutrophilic and Eosinophilic Inflammation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1324.

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cummings, steven M. "Fluorescein Isothiocyanate (FITC) Labelled Dextran As A Peripheral Marker Of Lung Inflammation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4376.

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Rotman, Oren, Dalit Shav, Uri Zaretsky, and Shmuel Einav. "Bio-Mechanical Aspects of Short Peripheral Catheter Thrombophlebitis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205445.

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Venflons, or Short Peripheral Catheters (SPC), are the most common intravenous devices being used in medical practice, particularly in hospitals and intensive care units. SPC is usually inserted into veins of the upper extremities to administer fluids, medications, blood products or for prophylactic use before procedures. It has been reported that 40–80% of hospitalized patients were treated with SPCs [1, 2]. Short Peripheral Catheter Thrombophlebitis (SPCT) is the most frequent complication of treatment with, characterized by pain, tenderness, warmth, erythema, swelling and palpable thrombosis of the cannulated vein. SPCT causes patients discomfort and generally leads to catheter removal and insertion of a new catheter at a different site [3]. SPCT is a sterile inflammation [2, 3], and its pathogenesis is not well understood. Several mechanisms have been suggested for SPCT pathogenesis, such as chemical irritation of the endothelium due to infusate or catheter material, or that vein wall injury combined with stasis cause an inflammation response and thrombosis [4, 5].
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Koloszko-Chomentowska, Zofia, and Leszek Sieczko. "Peripheral rural areas in face of challenges of sustainable development." In 17th International Scientific Conference Engineering for Rural Development. Latvia University of Agriculture, 2018. http://dx.doi.org/10.22616/erdev2018.17.n277.

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Jin, Seungwoo, AnBae Lee, ByounGyu Kim, IlSic Jang, JaeChun Cha, DongGoo Choi, Hyo Sang Kang, HyoYoung Kang, and SeonYong Cha. "Beyond 20nm DRAM peripheral transistor: Challenges and ion implantation solutions." In ION IMPLANTATION TECHNOLOGY 2012: Proceedings of the 19th International Conference on Ion Implantation Technology. AIP, 2012. http://dx.doi.org/10.1063/1.4766480.

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Shirai, Toshihiro, Masashi Mikamo, Yuichiro Shishido, Takefumi Akita, Satoru Morita, Kazuhiro Asada, Masato Fujii, Kazutaka Mori, Takafumi Suda, and Kingo Chida. "Colored 3D Analyses Of Respiratory Impedance In Asthma: Association With Peripheral Airway Inflammation And Dysfunction." 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.a3939.

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Mens, LJJ Van, SL Verweij, AWR van Kuijk, ESG Stroes, and DL Baeten. "FRI0464 Arterial wall inflammation is not affected by ANTI-IL17 treatment in patients with peripheral spondyloarthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4709.

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Lee, Yi Jae, Sung Jin Park, Ji Yoon Kang, and Soo Hyun Lee. "A cuff-shaped enzymeless glucose sensor integrated with chronically implantable peripheral nerve cuff electrode for inflammation monitoring." In 2015 7th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2015. http://dx.doi.org/10.1109/ner.2015.7146683.

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Reports on the topic "Peripheral challenges and inflammation"

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Lekhanya, Portia Keabetswe, and Kabelo Mokgalaboni. Exploring the effectiveness of vitamin B12 complex and alpha-lipoic acid as a treatment for diabetic neuropathy. Protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0167.

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Review question / Objective: Does Alpha-Lipoic acid increase the uptake of glucose for better glycaemic control? Does vitamin B12 and Alpha-Lipoic acid improve inflammation? The aim of the study is to explore the effectiveness of Vitamin B12 and Alpha-Lipoic Acid as a possible treatment for diabetic neuropathy with major emphasis on markers of inflammation and glucose metabolism. Condition being studied: Diabetic Neuropathy (DN) is a heterogeneous type of nerve damage associated with diabetes mellitus, the condition most often damages nerves in the legs and feet. It presents both clinically and sub-clinically affecting the peripheral nervous system as a result of an increase in glucose concentration which interferes with nerve signalling. After the discovery of insulin as a treatment for Diabetes Mellitus (DM), the prevalence of DN has since increased significantly due to DM patients having a longer life expectancy. It has been estimated that atleast 50% of DM patients will develop DN in their life, with approximately 20% of these patients experiencing neuropathic pain. Nerves are susceptible to changes in glucose concentrations and insulin makes it impossible for neurons to continue regulating glucose uptake.
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Mort, A. Controls on the distribution and composition of gas and condensate in the Montney resource play. Natural Resources Canada/CMSS/Information Management, 2022. http://dx.doi.org/10.4095/329790.

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The Montney resource play has evolved from a peripheral conventional play to one of the most important hydrocarbon-producing unconventional resource plays in North America and has remained resilient throughout the economic challenges of recent years. Despite maturing as a resource play as a result of more than 15 years of unconventional development and research there are still aspects of the play that are not fully de-risked and prediction of fluid quality remains haphazard due to the complex interplay of geological and engineering factors. Among these are the delineation of structural and stratigraphic barriers and conduits, identification of enigmatic source rocks, which defy traditional methods, evaluating effects of fluid migration and the difficulty in predicting phase behavior in a tight, but open system. This study uses a combined approach leveraging geochemical tools combined with spatial and stratigraphic analysis in an attempt to improve current understanding of these issues.
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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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