Modulation of Epithelial Cell Function by Glucocorticoids: Anti-Inflammatory and Other Effects

2008 ◽  
pp. 367-390
Author(s):  
Robert Newton ◽  
Manminder Kaur ◽  
Elizabeth M. King ◽  
Wei Gong ◽  
Donna M. Slater ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Function ◽  
Anti Inflammatory

Gut mucosa alterations and loss of segmented filamentous bacteria in type 1 diabetes are associated with inflammation rather than hyperglycaemia

Gut ◽  
2021 ◽  
pp. gutjnl-2020-323664 ◽  
Author(s):  
Matthieu Rouland ◽  
Lucie Beaudoin ◽  
Ophélie Rouxel ◽  
Léo Bertrand ◽  
Lucie Cagninacci ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Epithelial Cell ◽  
Cell Function ◽  
Diabetes Incidence ◽  
Filamentous Bacteria ◽  
Segmented Filamentous Bacteria ◽  
Gut Mucosa ◽  
Anti Inflammatory

ObjectiveType 1 diabetes (T1D) is an autoimmune disease caused by the destruction of pancreatic β-cells producing insulin. Both T1D patients and animal models exhibit gut microbiota and mucosa alterations, although the exact cause for these remains poorly understood. We investigated the production of key cytokines controlling gut integrity, the abundance of segmented filamentous bacteria (SFB) involved in the production of these cytokines, and the respective role of autoimmune inflammation and hyperglycaemia.DesignWe used several mouse models of autoimmune T1D as well as mice rendered hyperglycaemic without inflammation to study gut mucosa and microbiota dysbiosis. We analysed cytokine expression in immune cells, epithelial cell function, SFB abundance and microbiota composition by 16S sequencing. We assessed the role of anti-tumour necrosis factor α on gut mucosa inflammation and T1D onset.ResultsWe show in models of autoimmune T1D a conserved loss of interleukin (IL)-17A, IL-22 and IL-23A in gut mucosa. Intestinal epithelial cell function was altered and gut integrity was impaired. These defects were associated with dysbiosis including progressive loss of SFB. Transfer of diabetogenic T-cells recapitulated these gut alterations, whereas induction of hyperglycaemia with no inflammation failed to do so. Moreover, anti-inflammatory treatment restored gut mucosa and immune cell function and dampened diabetes incidence.ConclusionOur results demonstrate that gut mucosa alterations and dysbiosis in T1D are primarily linked to inflammation rather than hyperglycaemia. Anti-inflammatory treatment preserves gut homeostasis and protective commensal flora reducing T1D incidence.

II. One size fits all: nonclassical MHC molecules fulfill multiple roles in epithelial cell function

1998 ◽  
Vol 274 (2) ◽  
pp. G227-G231 ◽  
Author(s):  
Richard S. Blumberg
Keyword(s):  
Epithelial Cell ◽  
Mhc Class I ◽  
Cell Biology ◽  
Cell Function ◽  
Surface Glycoprotein ◽  
Class I ◽  
Human Major Histocompatibility Complex ◽  
Cell Surface Glycoprotein ◽  
Mhc Molecules ◽  
Nonclassical Mhc

The human major histocompatibility complex (MHC) on chromosome 6 encodes three classical class I genes: human leukocyte antigen-A (HLA-A), HLA-B, and HLA-C. These polymorphic genes encode a 43- to 45-kDa cell surface glycoprotein that, in association with the 12-kDa β2-microglobulin molecule, functions in the presentation of nine amino acid peptides to the T cell receptor of CD8-bearing T lymphocytes and killer inhibitory receptors on natural killer cells. In addition to these ubiquitously expressed polymorphic proteins, the human genome also encodes a number of nonclassical MHC class I-like, or class Ib, genes that in general encode nonpolymorphic molecules involved in a variety of specific immunologic functions. Many of these genes, including CD1, the neonatal Fc receptor for immunoglobulin G, HLA-G, the MHC class I chain-related gene A, and Hfe, are prominently displayed on epithelial cells, suggesting an important role in epithelial cell biology.

scholarly journals Pulmonary Epithelial Cell-Derived Cytokine TGF-β1 Is a Critical Cofactor for Enhanced Innate Lymphoid Cell Function

Immunity ◽  
2015 ◽  
Vol 43 (5) ◽  
pp. 945-958 ◽  
Author(s):  
Laura Denney ◽  
Adam J. Byrne ◽  
Thomas J. Shea ◽  
James S. Buckley ◽  
James E. Pease ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Lymphoid Cell ◽  
Cell Function ◽  
Innate Lymphoid Cell ◽  
Pulmonary Epithelial Cell ◽  
Tgf Β1

New Insights into Epithelial Cell Function in Mucosal Immunity

1996 ◽  
pp. 141-149 ◽  
Author(s):  
Michael E. Lamm ◽  
John G. Nedrud ◽  
Charlotte S. Kaetzel ◽  
Mary B. Mazanec
Keyword(s):  
Epithelial Cell ◽  
Mucosal Immunity ◽  
Cell Function

scholarly journals Inflammation in the Pathophysiology and Therapy of Cardiometabolic Disease

2019 ◽  
Vol 40 (4) ◽  
pp. 1080-1091 ◽  
Author(s):  
Marc Y Donath ◽  
Daniel T Meier ◽  
Marianne Böni-Schnetzler
Keyword(s):  
Metabolic Syndrome ◽  
Clinical Studies ◽  
Cell Function ◽  
Therapeutic Interventions ◽  
Metabolic Inflammation ◽  
Inflammatory Conditions ◽  
Β Cell Function ◽  
Associated Conditions ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Abstract The role of chronic inflammation in the pathogenesis of type 2 diabetes mellitus and associated complications is now well established. Therapeutic interventions counteracting metabolic inflammation improve insulin secretion and action and glucose control and may prevent long-term complications. Thus, a number of anti-inflammatory drugs approved for the treatment of other inflammatory conditions are evaluated in patients with metabolic syndrome. Most advanced are clinical studies with IL-1 antagonists showing improved β-cell function and glycemia and prevention of cardiovascular diseases and heart failure. However, alternative anti-inflammatory treatments, alone or in combinations, may turn out to be more effective, depending on genetic predispositions, duration, and manifestation of the disease. Thus, there is a great need for comprehensive and well-designed clinical studies to implement anti-inflammatory drugs in the treatment of patients with metabolic syndrome and its associated conditions.

Sign in / Sign up

Export Citation Format

Share Document