Biomechanical changes in oxazolone-induced colitis in BALB/C mice

Yang, Jimin; Zhao, Jingbo; Nakaguchi, Toshiya

doi:10.1016/j.jbiomech.2009.01.028

Cited by 16 publications

(15 citation statements)

References 31 publications

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“…This protective effect was shown to be even more striking upon close analysis of the colons. The oxazolone model of colitis typically affects the distal half of the colon [32] and leads to profound changes in the intestine, including colon shortening due to ulceration [38] and innate cell and lymphocyte infiltration to the superficial layer of the mucosa [11]. We found that neutralizing anti-IL-25 or anti-IL-17BR antibodies protected against this colon shortening, intestinal bleeding, and disruption of the mucosal structure.…”

Section: Discussionmentioning

confidence: 85%

“…Following these observations, we sought to look at the phenotypic changes in the intestine. One of the major macroscopic features of colitis in mice is the shortening of the colon that occurs due to ulceration and inflammation [38]. In order to assess the severity of colitis, we analyzed the macroscopic and microscopic appearance of the colons on day 2 post-challenge.…”

Section: Resultsmentioning

confidence: 99%

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Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13

et al. 2012

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BackgroundInterleukin-25 (IL-25) is a potent activator of type-2 immune responses. Mucosal inflammation in ulcerative colitis is driven by type-2 cytokines. We have previously shown that a neutralizing anti-IL-25 antibody abrogated airways hyperreactivity in an experimental model of lung allergy. Therefore, we asked whether blocking IL-25 via neutralizing antibodies against the ligand or its receptor IL-17BR could protect against inflammation in an oxazolone-induced mouse model of colitis.MethodsNeutralizing antibodies to IL-25 or IL-17BR were administered to mice with oxazolone-induced colitis, a model of ulcerative colitis. The disease onset was evaluated by weight loss and degree of colon ulceration. Also, lamina propria and mesenteric lymph node (MLN) infiltrates were assessed for mucosal inflammation and cultured in vitro to determine cytokine production.ResultsWe found that in oxazolone colitis IL-25 production derives from intestinal epithelial cells and that IL-17BR+ IL-13-producing natural killer T (NKT) cells and nuocytes drive the intestinal inflammation. Blocking IL-25 signalling considerably improved the clinical aspects of the disease, including weight loss and colon ulceration, and resulted in fewer nuocytes and NKT cells infiltrating the mucosa. The improved pathology correlated with a decrease in IL-13 production by lamina propria cells, a decrease in the production of other type-2 cytokines by MLN cells, and a decrease in blood eosinophilia and IgE.ConclusionIL-25 plays a pro-inflammatory role in the oxazolone colitis model, and neutralizing antibodies to IL-25 or IL-17BR can slow the ongoing inflammation in this disease. Because this model mimics aspects of human ulcerative colitis, these antibodies may represent potential therapeutics for reducing gut inflammation in patients.

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Section: Discussionmentioning

confidence: 85%

Section: Resultsmentioning

confidence: 99%

Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13

et al. 2012

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“…Various animal models have been established to study IBD; these broadly include chemical-induced colitis model, adoptive transfer model, model of spontaneous colitis, genetically engineered/transgenic animal model. Among these, the widely used models include chemical-induced colitis model that is sub-categorized into trinitrobenzene sulfonic acid (TNBS)-induced colitis [16,17,18], dextran sodium sulphate (DSS)-inducedcolitis [19,20,21], oxazolone-induced colitis [22,23,24], acetic acid-induced colitis [25,26,27,28], nonsteroidal anti-inflammatory drugs (NSAIDs)-induced colitis [29,30], carrageenan-induced colitis model [31,32], peptidoglycan-polysaccharide (PGPS)-induced colitis [33,34] (Table 1). Amongst the various models, chemical models are extensively used, as they offer reproducibility and ease of development.…”

Section: Introductionmentioning

confidence: 99%

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

Randhawa

Singh

et al. 2014

Korean J Physiol Pharmacol

385

310

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Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.

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“…The shortening of the colon that occurs due to ulceration and inflammation is an indicator of colitis severity in colitis mice [29]. As shown in Figure 3C, we observed shorter colons in the OXA mice than in the ETOH mice (8.58±1.20 vs. 11.05±0.70 cm, p <0.001).…”

Section: Resultsmentioning

confidence: 60%

CCL25/CCR9 Interactions Regulate the Function of iNKT Cells in Oxazolone-Induced Colitis in Mice

Zhu

Bing²,

Wang

et al. 2014

PLoS ONE

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BackgroundNatural killer T (NKT) cells share phenotypic and functional properties with both conventional natural killer cells and T cells. These cells might have an important role in the pathogenesis of ulcerative colitis (UC). The interaction of chemokine ligand 25 (CCL25) with chemokine receptor 9 (CCR9) is involved in gut-specific migration of leukocytes and induces regulatory T cells (Tregs) to migrate to the intestine in chronic ileitis.Methodology/FindingsIn UC patients, NKT receptor CD161, CCL25, and CCR9 expression levels were evaluated by qRT-PCR. A murine model of oxazolone-induced colitis was induced in BALB/c mice. The mRNA levels of NK1.1, CCL25 and CCR9, and pro-inflammatory cytokines in mice were evaluated. The CCR9 expression on Type I or invariant NKT (iNKT) cells, and the iNKT cells chemotaxis are observed according to flow cytometry. NKT receptor CD161, CCL25 and CCR9 expression levels were significantly increased in UC patients. And, the mRNA expression levels of NK1.1, CCL25 and CCR9 were increased in oxazolone-induced colitis in mice. The production of pro-inflammatory cytokines was significantly increased, especially interleukin 4 (IL-4), IL-10 and IL-13. We observed significantly increased CCR9 expression on iNKT cells. Furthermore, we found an increased iNKT population and enhanced chemotaxis during oxazolone-induced colitis.Conclusions/SignificanceOur study suggests that CCL25/CCR9 interactions may promote the induction and function of iNKT cells during oxazolone-induced colitis. These findings may have important implications for UC treatment and suggest a role for CCR9 inhibitors.

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Biomechanical changes in oxazolone-induced colitis in BALB/C mice

Cited by 16 publications

References 31 publications

Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13

Blocking IL-25 signalling protects against gut inflammation in a type-2 model of colitis by suppressing nuocyte and NKT derived IL-13

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

CCL25/CCR9 Interactions Regulate the Function of iNKT Cells in Oxazolone-Induced Colitis in Mice

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