Inflammation and cell signaling最新文献

{"title":"WHAT IS THE ROLE OF INFLAMMATORY MEDIATORS ON ENERGY METABOLISM","authors":"Simone Fátima Gomes","doi":"10.14800/ICS.1189","DOIUrl":"https://doi.org/10.14800/ICS.1189","url":null,"abstract":"The subclinical and low intensity inflammation, oxidative stress, high calorie and high fat diet patterns are striking features of the obesity. The adipose tissue, through its endocrine function, is associated with the cytokines secretion, such as: IL-4, IL-13, IL-15 and IFN-γ, which trigger metabolic changes and possibly modulate the energy metabolism by modifying the biochemical, anthropometric and body composition parameters. This review summarizes scientific evidences about the relationship between such cytokines and mediators which alter the energy metabolism, predisposing or preventing the obesity.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"53 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91445106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bilirubin acts as an endogenous regulator of inflammation by disrupting adhesion molecule-mediated leukocyte migration","authors":"Megan E. Vogel, S. Zucker","doi":"10.14800/ics.1178","DOIUrl":"https://doi.org/10.14800/ics.1178","url":null,"abstract":"There is a growing body of evidence that bilirubin, which is generated during the physiological breakdown of heme, exerts potent anti-inflammatory effects. Previous work by our group suggests that bilirubin is able to suppress inflammatory responses by preventing the migration of leukocytes into target tissues through disruption of vascular cell adhesion molecule-1 (VCAM-1)-dependent cell signaling. As VCAM-1 is an important mediator of tissue injury in the dextran sodium sulfate (DSS) murine model of inflammatory colitis, we examined whether bilirubin prevents colonic injury in DSS-treated mice. As anticipated, bilirubin-treated animals manifested significantly less colonic injury and reduced infiltration of inflammatory cells into colon tissues. We further observed that bilirubin administration was associated with a reduced number of eosinophils and monocytes in the small intestine, with a corresponding increase in peripheral blood eosinophilia, regardless of whether mice received DSS. These findings suggest that bilirubin impairs the normal migration of eosinophils into intestinal tissues, as supported by in vitro experiments showing that bilirubin blocks the VCAM-1-dependent movement of Jurkat cells across human endothelial cell monolayers. Taken together, our findings support that bilirubin ameliorates DSS-induced colitis and disrupts the physiological trafficking of leukocytes to the intestine by preventing transmigration across the vascular endothelium, potentially through the inhibition VCAM-1-mediated signaling. Our findings raise the possibility that bilirubin functions as an endogenous regulator of inflammatory responses.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87301055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assesment of Microcirculatory Function with Retrobulbar Blood Flow Velocity Measurement Predicting Cardiovascular Events","authors":"N. Keleş, M. Çalışkan, Necibe Nur Keles, F. Aksu, S. M. Aung","doi":"10.14800/ICS.1120","DOIUrl":"https://doi.org/10.14800/ICS.1120","url":null,"abstract":"Atherosclerosis first begins in the endothelium of the arterial wall, and is described as an inflammatory disease. Although atherosclerotic lesions occur in large arteries, the increased expression of adhesion molecules characteristic of endothelial cell activation, the decreased endothelium-dependent vasodilatation as well as oxidative stress are not limited to lesion-prone arteries where factors other than endothelial cell activation might progress to detect atheroma formation. Microvascular endothelial cell activation might be directly stimulated by cardiovascular risk factors with consequent release of inflammatory mediators and soluble isoforms of adhesion molecules that detect microvascular dysfunction and the atherosclerosis-associated systemic inflammatory state. The quantification of retrobulbar blood flow velocity has been used to analyze the microvascular circulation of the eye. Structural and functional changes in various microvascular beds can predict CV risk factors and diseases.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83757049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leptin-related polymorphisms and SLE","authors":"A. Cava","doi":"10.14800/ICS.1171","DOIUrl":"https://doi.org/10.14800/ICS.1171","url":null,"abstract":"Leptin is a hormone/cytokine that is mainly produced by adipocytes and has a range of actions that span from the control of metabolic balance to the modulation of adaptive and innate immune responses. Many investigations have indicated that the pro-inflammatory activities of leptin can contribute significantly to the promotion and maintenance of autoimmune responses. It is not known whether the abnormal elevation of leptin in patients with systemic lupus erythematous (SLE) - an autoimmune disease characterized by multi-organ involvement and the presence of autoantibodies – can reflect the chronic inflammatory status of the disease or contributes to the pathogenesis of the disease. To partly address this question, a recent investigation analyzed several leptin-related gene polymorphisms in SLE in large numbers of individuals from different ancestral groups. The study identified weak associations with certain SNPs that did not remain significant after correction for multiple testing. This review discusses the implications of those findings for the pathogenesis of SLE and for the possibility of leptin-based modalities of therapeutic intervention in the disease.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84353862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"p53/microRNAs signaling in the pathological mechanism of Diabetic Kidney Disease","authors":"Can Wu, Qiuyue Wang","doi":"10.14800/ICS.1132","DOIUrl":"https://doi.org/10.14800/ICS.1132","url":null,"abstract":"Recent studies found that high glucose increases the expression of tumor suppressor factor p53. And in the process of diabetic kidney disease (DKD) development p53 involves in regulating multiple signaling pathways. In addition, microRNAs (miRNAs) involve in many diseases pathogenesis. And miRNAs affect DKD development via adjusting multiple mechanism. More importantly, p53/miRNAs signaling may participate in a variety of signaling pathways regulating kidney inflammation and fibrosis to control DKD pathological development. However, the mechanism of p53/miRNAs signaling participate in DKD pathological development is not yet clear. To illuminate the role of p53/miRNAs signaling may inspire a new thinking for elucidating the pathological mechanism of DKD, and provide a new theoretical basis for the prevention and treatment of DKD.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78721620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intestinal RORrt-generated Th17 cells control type 2 diabetes: A first antidiabetic target identified from the host to microbiota crosstalk","authors":"Céline Pomié, L. Garidou, R. Burcelin","doi":"10.14800/ICS.1074","DOIUrl":"https://doi.org/10.14800/ICS.1074","url":null,"abstract":"The recent discovery of the role played by gut microbiota on the control of metabolic disease opens novel routes for the identification of the causes of type 2 diabetes and obesity. This paradigm could explain the infiltration, by innate and adaptive immune cells, of the adipose tissue, liver, and islets of Langerhans which is responsible for the metabolic inflammation state that leads to impaired insulin action and secretion, and therefore, type 2 diabetes. The identification of the causal role of circulating lipopolysaccharides LPS and peptidoglycans in the development of metabolic inflammation, due to an increased intestinal permeability, led to the leaky gut hypothesis. In addition, whole live bacteria were found in metabolic tissues establishing a tissue microbiota which upon a fat-enriched diet becomes dysbiotic. The process of intestinal bacterial translocation was responsible for the onset of a leaky gut causal to the disease. The translocation of selective sets of intestinal bacteria to the blood could be identified. These blood bacterial 16SrRNA-DNA sequences are considered as biomarkers of the bacterial translocation process. An increased of the corresponding bacterial DNA concentration was predicting the occurrence of type 2 diabetes. Associated to the dysbiotic microbiota translocation, an impaired intestinal immune defense was identified as a cause of the selective leaky gut. The change in small intestine mucosal microbiota induced by a fat-enriched diet reduces the number of IL17-secreting CD4 T cells within the lamina propria of the intestine. This loss of IL17-secreting CD4 T cells is the consequence of an impaired capacity of intestinal antigen presenting cells to activate and trigger the expression of RORgt and the production of IL17 by CD4 T cells. Altogether, an impaired intestinal immune defense, notably the reduced differentiation of RORgt expressing IL17-producing CD4 T cells, favors the onset of a leaky gut leading to the translocation of bacterial factors and live bacteria towards tissues triggering metabolic inflammation; insulin resistance and type 2 diabetes. Hence, the triggering of intestinal defense surrounding RORgt pathway now appears as a potential target mechanism for the control of type 2 diabetes.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74281978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aryl hydrocarbon receptor signaling involves in the human intestinal ILC3/ILC1 conversion in the inflamed terminal ileum of Crohn's disease patients.","authors":"Jian Li,&nbsp;Andria Doty,&nbsp;Sarah C Glover","doi":"10.14800/ics.1404","DOIUrl":"https://doi.org/10.14800/ics.1404","url":null,"abstract":"<p><p>Innate lymphoid cells (ILCs) are emerging as important components of our immune system that have critical effector and regulatory functions in both innate and adaptive immune responses. They are enriched at mucosal surfaces, such as lung and intestine. Our previous work has shown that Lineage^-CRTH2^-CD45⁺NKp44^-CD117^-CD127⁺ILC1s accumulated in the inflamed terminal ileum of patients with Crohn's disease (CD) at the expense of NKp44⁺ILC3s. This phenotype conversion impairs the intestinal barrier integrity and contributes to the dysregulated immune responses of CD patients. Our next step was to search for pathways to modulate this phenotype switch. The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor. Initial studies of AHR concentrated on its role in the detoxification of xenobiotics. However, recent research has focused on the immune system. Especially, AHR pathway is proven to be essential for the maintenance of intestinal ILC3s in mouse models. We examined whether AHR pathway participated in the human intestinal ILC phenotype change in the inflamed terminal ileum of CD patients. As anticipated, NKp44⁺ILC3s, NKp44^-ILC3s and ILC1s had differential AHR expression. This AHR signaling mediated CD117 expression on the surface of ILC3s. The conversion from ILC3 to ILC1 was accompanied by the downregulation of AHR expression. We further observed that there was a disparity between AHR protein expression and mRNA expression in the inflamed terminal ileum tissues of CD patients compared to unaffected areas. These findings suggest that AHR pathway is also important for human intestinal ILC phenotype regulation and impaired AHR signaling in the inflamed gut of CD patients possibly contributes to the ILC3/ILC1 conversion.</p>","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5341615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34806100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antacid therapy and disease outcomes in idiopathic pulmonary fibrosis: flip side of the story.","authors":"Yohannes T Ghebre","doi":"10.14800/ics.1397","DOIUrl":"10.14800/ics.1397","url":null,"abstract":"","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749412/pdf/nihms920317.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35710328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood borne: bacterial components in mother's blood influence fetal development.","authors":"Allister J Loughran,&nbsp;Elaine I Tuomanen","doi":"10.14800/ics.1421","DOIUrl":"https://doi.org/10.14800/ics.1421","url":null,"abstract":"<p><p>Bacterial or viral infection of the mother during the course of pregnancy can cross the placenta and actively infect the fetus. However, especially for bacteria, it is more common for mothers to experience an infection that can be treated without overt fetal infection. In this setting, it is less well understood what the risk to fetal development is, particularly in terms of neurological development. This research highlight reviews recent findings indicating that bacterial components generated during infection of the mother can cross the placenta and activate the fetal innate immune system resulting in changes in the course of brain development and subsequent progression to postnatal cognitive disorders. Bacterial cell wall is a ubiquitous bacterial PAMP (pathogen-associated molecular pattern) known to activate inflammation through the stimulation of TLR2. Cell wall is released from bacteria during antibiotic treatment and new work shows that embryos exposed to cell wall from the mother demonstrate anomalous proliferation of neuronal precursor cells in a TLR2 dependent manner. Such proliferation increases the neuronal density of the cortical plate and alters brain architecture. Although there is no fetal death, subsequent cognitive development is significantly impaired. This model system suggests that bacterial infection of the mother and its treatment can impact fetal brain development and requires greater understanding to potentially eliminate a risk factor for cognitive disorders such as autism.</p>","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5340199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34800994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autotaxin signaling, purinergic receptors and lung damage","authors":"J. Högberg","doi":"10.14800/ICS.1092","DOIUrl":"https://doi.org/10.14800/ICS.1092","url":null,"abstract":"ATX is a secreted enzyme that produces lysophosphatindic acid (LPA) in plasma. For several years investigators have characterize endogenous factors that regulate ATX expression and compartmentalization. However many questions remain unanswered and this article highlights our recent finding that autotaxin (ATX) is readily induced by toxic environmental chemicals. LPA binds G-protein coupled receptors that affect basic cell functions. The interest in the ATX-LPA axis stems from its role in embryogenesis and its association to diseases such as allergic asthma, idiopathic lung fibroses, rheumatoid arthritis, wound healing and several common types of cancer. In our study we used toluene diisocyanate (TDI) and other diisocyanates. Diisocyanates are low-molecular weight industrial chemicals notorious for being respiratory sensitizers and lung toxicants. Mechanisms behind these effects are not sufficiently characterized. We mainly used TDI and found that TDI in the nM range induced a rapid secretion of ATX from respiratory epithelial cells. Two purinergic recptors, P2X4 and P2X7, were implicated in this effect of TDI, suggesting that there is a “P2X-ATX axis” in bronchial epithelium that is sensitive to diisocyanates. We also showed associations between TDI exposures, LPA levels in plasma and symptoms reported by exposed individuals. Thus, our data support a role for the ATX-LPA axis in TDI toxicity. Furthermore, they suggest novel ways to study the regulation of ATX expression. Of particular interest is to understand how ATX expression is affected by purinergic receptors, and to investigate a possible involvement of ATX in asthma induced by diisocyanates and perhaps other low-molecular weight environmental chemicals. Our study also raises questions about current occupational exposure limits for diisocyanates.","PeriodicalId":13679,"journal":{"name":"Inflammation and cell signaling","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78775377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}