O-009 Lymphotoxin Links Microbiota and Group 3 Innate Lymphoid Cells to Protect Against Intestinal Inflammation

Koroleva, Ekaterina P.; Muraoka, Wayne; Spencer, Cody M.; Gubernatorova, Ekaterina O.; Halperin, Sydney; Snapper, Scott B.; Tumanov, Alexei V.

doi:10.1097/01.mib.0000480047.19127.68

Cited by 2 publications

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“…In acute colonic infections, such as Citrobacter rodentium , where rapid repair of colonic epithelial cells is required, IL22 plays a protective role 3 4. Likewise, IL22 facilitates epithelial restitution after induction of acute injury after short-term exposure to the detergent DSS, which results in abrupt tissue injury that rapidly resolves shortly after removal of the chemical insult 5 6. Administration of the chemotherapy agent methotrexate also induces a self-resolving mucositis characterised by acute small intestinal epithelial damage, in which IL22 plays an important restorative role 7.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-22 orchestrates a pathological endoplasmic reticulum stress response transcriptional programme in colonic epithelial cells

Powell

Pantazi

Pavlidis

et al. 2019

Gut

100

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Figure 1 IL22 induces an ER stress/unfolded protein response transcriptional module in colonic epithelial cells. (A) Heat map demonstrating pathway specific transcript expression in murine colonoids treated with (+IL22, n=3) or without (control, n=3) recombinant IL22. Mouse gene 2.0 ST array platform (affymetrix). (B) GSEA evaluating enrichment of ER stress response transcriptional module in IL22 treated colonoids. A core set of colonic epithelial-specific ER stress genes was defined by analysing significantly differentially expressed (p<0.05 and absolute value of the log2 fold change >±2) transcripts in colonoids treated with tunicamycin (n=3) or medium alone (n=3). (C) Expression of ER stress response transcripts in IL22 treated WT and Il22ra1 −/− colonoids (RNA-seq dataset ERR247358-ERR247389, Pham et al, 2014). 18 (D) Enrichment analysis for ER stress-related functional annotation groups (GO biological processes) in IL22-treated colonoids from dataset ERR247358-ERR247389. (E) Microarray analysis of core ER stress response transcripts in colonoids treated with tunicamycin (n=3), tunicamycin+IL22 (n=3) or untreated (control, n=3). (F) Real-time PCR quantification of ER stress transcripts in colonoids treated with IL22 (n=11), IL17A (n=6) and IL22+IL17A (n=6) and unexposed controls. *P<0.01. (G) Immunoblot and densitometry quantification (H) detecting GRP78 protein expression in colonoids treated with different cytokines. *P<0.026, one tailed t test. ER, endoplasmic reticulum; GO, Gene Ontology; GSEA, Gene Set Enrichment Analysis; IL22, interleukin-22.on July 6, 2020 by guest. Protected by copyright.

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Section: Introductionmentioning

confidence: 99%

Interleukin-22 orchestrates a pathological endoplasmic reticulum stress response transcriptional programme in colonic epithelial cells

Powell

Pantazi

Pavlidis

et al. 2019

Gut

100

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“…It is produced by several cell types but principally by ILC3s, and it has been shown to promote intestinal epithelial cell homeostasis and wound healing through STAT3 activation [ 45 ]. In addition, interaction of surface LT on ILC3s with LT β R on intestinal epithelial cells can lead to IL-22 production in colon in C. rodentium and DSS-induced colitis models [ 78 ]. The production of IL-22 by ILCs is induced by IL-23, which is associated with different models of colitis and human IBD [ 16 , 36 ].…”

Section: Cross Talk Between Epithelium and Ilcmentioning

confidence: 99%

When Insult Is Added to Injury: Cross Talk between ILCs and Intestinal Epithelium in IBD

Gracht

Zahner

Kronenberg

2016

Mediators of Inflammation

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Inflammatory bowel disease (IBD) is characterized by an impairment of the integrity of the mucosal epithelial barrier, which causes exacerbated inflammation of the intestine. The intestinal barrier is formed by different specialized epithelial cells, which separate the intestinal lumen from the lamina propria. In addition to its crucial role in protecting the body from invading pathogens, the intestinal epithelium contributes to intestinal homeostasis by its biochemical properties and communication to underlying immune cells. Innate lymphoid cells (ILCs) are a recently described population of lymphocytes that have been implicated in both mucosal homeostasis and inflammation. Recent findings indicate a critical feedback loop in which damaged epithelium activates these innate immune cells to restore epithelial barrier function. This review will focus on the signalling pathways between damaged epithelium and ILCs involved in repair of the epithelial barrier and tissue homeostasis and the relationship of these processes with the control of IBD.

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O-009 Lymphotoxin Links Microbiota and Group 3 Innate Lymphoid Cells to Protect Against Intestinal Inflammation

Cited by 2 publications

References 0 publications

Interleukin-22 orchestrates a pathological endoplasmic reticulum stress response transcriptional programme in colonic epithelial cells

Interleukin-22 orchestrates a pathological endoplasmic reticulum stress response transcriptional programme in colonic epithelial cells

When Insult Is Added to Injury: Cross Talk between ILCs and Intestinal Epithelium in IBD

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