Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines

Dieleman, Levinus A.; Palmen, Mary; Akol, Halil; Bloemena, Elisabeth; Peña, A. S.; Meuwissen, S. G. M.; Rees, E. P. Van

doi:10.1046/j.1365-2249.1998.00728.x

Cited by 961 publications

(775 citation statements)

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“…In addition, inhibition of endogenous IFN g by antibodies has been shown to ameliorate the chronic stage of colitis, indicating that IFN g is likely a key mediator for intestinal inflammation. 28 Here, we demonstrated that IFN g increases CD98 glycoprotein expression in Caco2-BBE monolayers. This observation is consistent with the CD98 upregula- …”

Section: Discussionmentioning

confidence: 61%

Activation of epithelial CD98 glycoprotein perpetuates colonic inflammation

Kucharzik

Lügering

Yan

et al. 2005

Laboratory Investigation

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Anomalies in the regulation and function of integrins have been implicated in the etiology of various pathologic conditions, including inflammatory disorders such as irritable bowel disease. Several classes of cell surface glycoproteins such as CD98 have been shown to play roles in integrins-mediated events. Here, we investigated the role of CD98 in intestinal inflammation using both in vivo and in vitro approaches. We found that in Caco2-BBE monolayers and colonic tissues, expression of CD98 was upregulated by the proinflammatory cytokine, interferon gamma (INF c). Furthermore, CD98 was highly upregulated in colonic tissues from mice with active colitis induced by dextran sodium sulfate (DSS), but not in DSS-treated INF c À/À mice. Administration of an anti-CD98 antibody worsened DSS-induced colitis in mice but had no effect on untreated control mice. Finally, we used Caco2-BBE cell monolayers to model intestinal epithelial wound healing, and found that activation of epithelial CD98 in DSS-treated monolayers inhibited monolayer reconstitution, but had no affect on untreated control monolayers. Our data collectively indicate that (i) CD98 upregulation is mediated by INF c during intestinal inflammation and (ii) activation of epithelial CD98 protein aggravates intestinal inflammation by reducing intestinal epithelial reconstitution. Overall, our data suggest that epithelial CD98 plays an important role in the perpetuation of intestinal inflammation. Laboratory Investigation (2005) 85, 932-941.

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Section: Discussionmentioning

confidence: 61%

Activation of epithelial CD98 glycoprotein perpetuates colonic inflammation

Kucharzik

Lügering

Yan

et al. 2005

Laboratory Investigation

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“…WT mice showed a weak, polarized Th1 response during the acute disease phase and a mixed Th1/Th2 response during the chronic phase of the inflammation, as described [32,37]. In contrast, CCR6-deficient mice did not show a specific Th1 response, as basal IFN-+ mRNA levels in colon, which are about twofold higher than those of WT mice, did not increase in either the acute or the chronic phase of DSS-induced colitis.…”

Section: Discussionmentioning

confidence: 78%

CCR6 has a non‐redundant role in the development of inflammatory bowel disease

et al. 2003

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Antigen-loaded tissues such as the intestinal mucosa must simultaneously elicit appropriate immune response to innocuous bacteria and food proteins, and to potentially harmful antigens. Impairment of the mechanisms controlling this response may mediate the excessive immune reaction that can lead to tissue destruction and inflammatory intestinal diseases, including inflammatory bowel disease. The intestinal epithelium influences local immune responses through the expression of adhesion molecules, costimulatory factors, cytokines and chemokines. CCL20, a g -chemokine expressed in epithelia from colon and other intestinal tissue, plays a role in immune responses of intestinal mucosa, as deduced from the defects in intestinal leukocyte homeostasis shown by mice lacking CCR6, the CCL20 receptor. We studied the response of CCR6-deficient mice in two models of inflammatory bowel disease. The data show that absence of CCR6 resulted in less severe intestinal pathology in animals treated with dextran sodium sulfate. Conversely, CCR6 deficiency alters leukocyte homeostasis and the cytokine environment in the intestinal mucosa; these changes are sufficient to confer susceptibility to trinitrobenzene sulfonic acid-induced intestinal inflammation in the otherwise resistant C57BL/6J mouse strain. These results suggest that the CCR6/ CCL20 axis has a critical, non-redundant role in the in vivo control of immune responses in the intestine.

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“…Induction and evaluation of DSS-induced colitis were performed according to the previous reports [26][27][28]45,46 with some modifications. In brief, mice were given 2% DSS (molecular weight 36,000-50,000; ICN Biomedicals, Burlington, ON, Canada) dissolved in sterile distilled water for 7 days.…”

Section: Methodsmentioning

confidence: 99%