The Role of CXCR3 in DSS-Induced Colitis

Chami, Belal; Yeung, Amanda W. S.; Vreden, Caryn van; King, Nicholas J. C.; Bao, Shisan

doi:10.1371/journal.pone.0101622

Cited by 56 publications

(46 citation statements)

References 51 publications

(61 reference statements)

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“…Increased proliferation of epithelial cells contributes to this effect (47). Consistently, loss of the CXCL10 receptor, CXCR3, strongly protected mice from DSS-induced colitis (48). Based on these results, anti-CXCL10 treatment appears as an attractive option for clinical therapy.…”

Section: Discussionmentioning

confidence: 81%

Noncanonical Effects of IRF9 in Intestinal Inflammation: More than Type I and Type III Interferons

Rauch

Rosebrock

Hainzl

et al. 2015

Molecular and Cellular Biology

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Section: Discussionmentioning

confidence: 81%

Noncanonical Effects of IRF9 in Intestinal Inflammation: More than Type I and Type III Interferons

Rauch

Rosebrock

Hainzl

et al. 2015

Molecular and Cellular Biology

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“…157,158 CXCR3-deficient mice are resistant to DSS-induced colitis. 159 CXCR3 and its ligands CXCL9, CXCL10, and CXCL11 are reportedly overexpressed in pediatric and adult patients with IBD. 160,161 …”

Section: Trafficking Blockade and Intestinal Inflammationmentioning

confidence: 99%

Leukocyte Trafficking to the Small Intestine and Colon

et al. 2016

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Leukocyte trafficking to the small and large intestines is tightly controlled to maintain intestinal immune homeostasis, mediate immune responses, and regulate inflammation. A wide array of chemoattractants, chemoattractant receptors, and adhesion molecules expressed by leukocytes, mucosal endothelium, epithelium, and stromal cells controls leukocyte recruitment and microenvironmental localization in intestine and in the gut-associated lymphoid tissues (GALTs). Naive lymphocytes traffic to the gut-draining mesenteric lymph nodes where they undergo antigen-induced activation and priming; these processes determine their memory/effector phenotypes and imprint them with the capacity to migrate via the lymph and blood to the intestines. Mechanisms of T-cell recruitment to GALT and of T cells and plasmablasts to the small intestine are well described. Recent advances include the discovery of an unexpected role for lectin CD22 as a B-cell homing receptor GALT, and identification of the orphan G-protein–coupled receptor 15 (GPR15) as a T-cell chemoattractant/trafficking receptor for the colon. GPR15 decorates distinct subsets of T cells in mice and humans, a difference in species that could affect translation of the results of mouse colitis models to humans. Clinical studies with antibodies to integrin α4β7 and its vascular ligand mucosal vascular addressin cell adhesion molecule 1 are proving the value of lymphocyte trafficking mechanisms as therapeutic targets for inflammatory bowel diseases. In contrast to lymphocytes, cells of the innate immune system express adhesion and chemoattractant receptors that allow them to migrate directly to effector tissue sites during inflammation. We review the mechanisms for innate and adaptive leukocyte localization to the intestinal tract and GALT, and discuss their relevance to human intestinal homeostasis and inflammation.

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“…CXCR2-deficient mice display a lower susceptibility to acute and chronic colitis induced by DSS, with less inflammatory cell infiltration and less ulcer formation [38,39]. Similarly, blocking CXCR2 with antibodies or with antagonists dampens colitis [39,40], as knockdown or blockage of some other CCR and CXC receptors [41,42,43]. …”

Section: Effects Of Targeting Neutrophil Chemotaxis and Extravasationmentioning

confidence: 99%

The Dual Role of Neutrophils in Inflammatory Bowel Diseases

Wéra

Lancellotti

Oury

2016

JCM

210

164

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Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are characterised by aberrant immunological responses leading to chronic inflammation without tissue regeneration. These two diseases are considered distinct entities, and there is some evidence that neutrophil behaviour, above all other aspects of immunity, clearly separate them. Neutrophils are the first immune cells recruited to the site of inflammation, and their action is crucial to limit invasion by microorganisms. Furthermore, they play an essential role in proper resolution of inflammation. When these processes are not tightly regulated, they can trigger positive feedback amplification loops that promote neutrophil activation, leading to significant tissue damage and evolution toward chronic disease. Defective chemotaxis, as observed in Crohn’s disease, can also contribute to the disease through impaired microbe elimination. In addition, through NET production, neutrophils may be involved in thrombo-embolic events frequently observed in IBD patients. While the role of neutrophils has been studied in different animal models of IBD for many years, their contribution to the pathogenesis of IBD remains poorly understood, and no molecules targeting neutrophils are used and validated for the treatment of these pathologies. Therefore, it is crucial to improve our understanding of their mode of action in these particular conditions in order to provide new therapeutic avenues for IBD.

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The Role of CXCR3 in DSS-Induced Colitis

Cited by 56 publications

References 51 publications

Noncanonical Effects of IRF9 in Intestinal Inflammation: More than Type I and Type III Interferons

Noncanonical Effects of IRF9 in Intestinal Inflammation: More than Type I and Type III Interferons

Leukocyte Trafficking to the Small Intestine and Colon

The Dual Role of Neutrophils in Inflammatory Bowel Diseases

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