Amelioration of dextran sulfate sodium–induced colitis by anti-macrophage migration inhibitory factor antibody in mice

Ohkawara, Tatsuya; Nishihira, Jun; Takeda, Hiroshi; Hige, Shuhei; Kato, Mototsugu; Sugiyama, Toshiro; Iwanaga, Toshihiko; Nakamura, Hideki; Mizue, Yuka; Asaka, Masahiro

doi:10.1053/gast.2002.34236

Cited by 136 publications

(141 citation statements)

References 41 publications

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“…9,54 Mononuclear cell infiltration was analyzed indirectly by measuring NAG activity. Colon tissues had a high number of resident mononuclear cells, which was significantly enhanced 7 days after DSS administration.…”

Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

Bento

Marcon

Dutra

et al. 2011

The American Journal of Pathology

208

145

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Cannabinoid receptor 2 (CB2) activation is suggested to trigger the peroxisome proliferator-activated receptor-␥ (PPAR␥) pathway, and agonists of both receptors improve colitis. Recently, the plant metabolite (E)-␤-caryophyllene (BCP) was shown to bind to and activate CB2. In this study, we examined the antiinflammatory effect of BCP in dextran sulfate sodium (DSS)-induced colitis and analyzed whether this effect was mediated by CB2 and PPAR␥. Oral treatment with BCP reduced disease activity, colonic macro-and microscopic damage, myeloperoxidase and N-acetylglucosaminidase activities, and levels and mRNA expression of colonic tumor necrosis factor-␣, IL-1␤, interferon-␥, and keratinocyte-derived chemokine. Inflammatory bowel diseases (IBDs) are a group of chronic diseases that affect the gastrointestinal tract and have been mainly subdivided as ulcerative colitis and Crohn's disease. 1 The IBDs are characterized by a strong leukocyte activation and infiltration into the intestinal tissues, the release of proinflammatory cytokines 2 and enzymes, and the formation of reactive oxygen species. All of these events can induce an extensive and unbalanced activation of the mucosal immune system, driven by the commensal flora. 3 Recent evidence suggests a role for the cannabinoid system in IBD regulation. Cannabinoid receptors 1 and 2 (CB1 and CB2) are expressed in normal human colon 4,5 and are up-regulated in IBD colonic tissue. In addition, an enhanced level of endocannabinoids was found in biopsy specimens from patients with ulcerative colitis. 5 It is thought that CB1 activation results in a decrease of intestinal hypermotility and hypersecretion, whereas the activation of CB2 results in the inhibition of proinflammatory mediators. In addition, both CB2 and CB1 knockout mice are more susceptible to the development of experimental colitis, and the activation of these receptors is extremely important for the abrogation of intestinal inflammation. 6 The role of CB2, however, is directly involved with innate immune system, because CB2 is primarily expressed in immune cells, such as macrophages, CD4 ϩ and CD8 ϩ T cells, monocytes, and polymorphonuclear neutro-

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Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

Bento

Marcon

Dutra

et al. 2011

The American Journal of Pathology

208

145

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“…Administration of DSS to induce subclinical colitis, while convenient, does not yield a model that perfectly mimics the pathogenesis of IBD, since DSS causes a chemical colitis through epithelial injury. 26 Nevertheless, DSS has been commonly used to study the pathogenesis of colitis 18,[26][27][28][29][30][31] and was useful to allow us to model the clinical scenarios of ETBF colonization preceding or following the emergence of colitis in the host. Another potential study limitation was the use of antibiotics to enhance bacterial colonization.…”

Section: Discussionmentioning

confidence: 99%

Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis

Rabizadeh

Rhee

et al. 2007

Inflammatory Bowel Diseases

121

102

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Background-Inflammatory bowel disease (IBD) is proposed to result from a dysregulated mucosal immune response to the colonic flora in genetically susceptible individuals. Enterotoxigenic Bacteroides fragilis (ETBF), a molecular subclass of the common human commensal, B. fragilis, has been associated with IBD. This study investigated whether ETBF colonization of mice initiated colitis or modified the clinical course of a colitis agonist, dextran sodium sulfate (DSS).

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“…Histopathology was determined from sections of fixed lungs stained with H&E, PAS, or rabbit-anti-rat/ mouse MIF polyclonal antiserum. Rabbit anti-rat/mouse MIF antiserum was generated at our facility as described previously [51] and used for staining after protein A Sepharose purification.…”

Section: Methodsmentioning

confidence: 99%

Thioredoxin suppresses airway inflammation independently of systemic Th1/Th2 immune modulation

Torii

Wang

et al. 2010

Eur J Immunol

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Oxidative stress plays an important role in the pathogenesis of asthma via the upregulation of local inflammatory mediators and/or promoting Th2-skewing during Ag sensitization. Thioredoxin (TRX), a 12 kDa redox-active protein with antioxidative property, has been recently shown to play a protective role in various inflammatory diseases. Using a mouse model of asthma, we show here that IL-13 and eotaxin production are decreased in TRX-Tg mice leading to reduced eosinophils recruitment and mucus metaplasia. The reduction in airway inflammation occurs without the attenuation of systemic Th2 immunity in that comparable levels of Th2-type cytokines and Ig were detected in LN and serum, respectively, from TRX-Tg and WT mice. Likewise, CD4 1 T cells from both strains of mice developed similar Th1 and Th2 responses in vitro. Asthmatic lungs of TRX-Tg and WT mice contained similar amounts of GATA-3 1 and Foxp3 1 T cells. Finally, production of MIF, an upstream modulator of airway inflammation, was significantly reduced in the lungs of TRX-Tg mice. Our data suggest that TRX suppresses airway inflammation by inhibiting MIF production thereby limiting the downstream recruitment of eosinophils to the lung independently of modulating systemic Th1/Th2 immunity.

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Amelioration of dextran sulfate sodium–induced colitis by anti-macrophage migration inhibitory factor antibody in mice

Cited by 136 publications

References 41 publications

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

β-Caryophyllene Inhibits Dextran Sulfate Sodium-Induced Colitis in Mice through CB2 Receptor Activation and PPARγ Pathway

Enterotoxigenic Bacteroides fragilis: A potential instigator of colitis

Thioredoxin suppresses airway inflammation independently of systemic Th1/Th2 immune modulation

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