Distribution of mast cells, macrophages of colonic mucosa of patients with collagenous colitis and inflammatory bowel disease

Yu, Ning; Murase, Kunihiko; Furusu, Hisashi; Isomoto, Hiroharu; Takeshima, Fuminao; Mizuta, Youhei; Hewlett, Br.; Riddell, R H; Kohno, Shigeru

doi:10.1016/s0016-5085(98)84277-7

Cited by 42 publications

(54 citation statements)

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“…Most experts agree that IBD is a consequence of abnormal immune responses to intestinal lumen pathogens and exogenous antigens (25). Because increased numbers of activated and degranulating MCs have been found in IBD patients (26,27), we hypothesized that MCs and one or more of their granule protease mediators Fig. 6.…”

Section: Discussionmentioning

confidence: 99%

Essential role for mast cell tryptase in acute experimental colitis

Hamilton

Sinnamon

Lyng³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

110

102

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Patients with inflammatory bowel disease (IBD) have increased numbers of human tryptase-β (hTryptase-β)-positive mast cells (MCs) in the gastrointestinal tract. The amino acid sequence of mouse mast cell protease (mMCP)-6 is most similar to that of hTryptase-β. We therefore hypothesized that this mMCP, or the related tryptase mMCP-7, might have a prominent proinflammatory role in experimental colitis. The dextran sodium sulfate (DSS) and trinitrobenzene sulfonic acid (TNBS) colitis models were used to evaluate the differences between C57BL/6 (B6) mouse lines that differ in their expression of mMCP-6 and mMCP-7 with regard to weight loss, colon histopathology, and endoscopy scores. Microarray analyses were performed, and confirmatory real-time PCR, ELISA, and/or immunohistochemical analyses were carried out on a number of differentially expressed cytokines, chemokines, and matrix metalloproteinases (MMPs). The mMCP-6-null mice that had been exposed to DSS had significantly less weight loss as well as significantly lower pathology and endoscopy scores than similarly treated mMCP-6-expressing mice. This difference in colitis severity was confirmed endoscopically in the TNBS-treated mice. Evaluation of the distal colon segments revealed that numerous proinflammatory cytokines, chemokines that preferentially attract neutrophils, and MMPs that participate in the remodeling of the ECM were all markedly increased in the colons of DSS-treated WT mice relative to untreated WT mice and DSS-treated mMCP-6-null mice. Collectively, our data show that mMCP-6 (but not mMCP-7) is an essential MC-restricted mediator in chemically induced colitis and that this tryptase acts upstream of many of the factors implicated in IBD.

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Section: Discussionmentioning

confidence: 99%

Essential role for mast cell tryptase in acute experimental colitis

Hamilton

Sinnamon

Lyng³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

110

102

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“…16,17 Mediators such as CCL5, LTB 4 , and LTC 4 have also been implicated in models of local eosinophilic inflammation and may have a role in the eosinophilic response noted in DSS colitis. 7 In other models of pathogen-induced eosinophilia, it has been shown that direct stimulation of TLR2 by M. bovis can induce an eosinophilic infiltration into the pleural cavity that is highly dependent on IL-5, CCL11, and the CCL11 receptor CCR3.…”

Section: Discussionmentioning

confidence: 99%

“…Notably, mast cells were not found to contribute substantially to the regulation of eosinophils in DSS colitis, although they have been shown to be pivotal for eosinophilic responses in models of allergic disease. Studies using airway administration of chitin demonstrated lung eosinophilic inflammation that was independent of both TLRs and mast cells, but highly dependent on LTB 4 . 51 Taken together with the present data, these findings suggest the existence of multiple distinct pathways whereby local tissue eosinophilia can be induced.…”

Section: Discussionmentioning

confidence: 99%

“…A cellular infiltrate composed of several cell types, including eosinophils neutrophils, monocytes, and mast cells, is associated with intestinal inflammation in these inflammatory bowel diseases (IBD). [1][2][3][4] Eosinophils are multifunctional leukocytes frequently mobilized during T helper 2 (Th2)-driven processes, such as allergic responses and parasitic helminth infections. In these contexts, eosinophils have been implicated in the pathogenesis of disease.…”

mentioning

confidence: 99%

“…[37][38][39] Specifically, in the gastrointestinal tract mucosal mast cells can produce significant amounts of IL-5, CCL11, and LTC 4 after IgE-mediated stimulation, making them key cells to study in disease processes associated with eosinophilia. 40 Mast cells also express TLR2 and can produce cytokines and lipid mediators (eg, TNF, IL-5, IL-13, LTB 4 , and LTC 4 ) in response to TLR2 activation. [41][42][43] The role of mast cells has not been considered in detail in the DSS model of colitis.…”

mentioning

confidence: 99%

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Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

Albert

Duplisea

Dawicki

et al. 2011

The American Journal of Pathology

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The mechanisms initiating eosinophil influx into sites of inflammation have been well studied in allergic disease but are poorly understood in other settings. This study examined the roles of TLR2 and mast cells in eosinophil accumulation during a nonallergic model of eosinophilia-associated colitis. TLR2-deficient mice (TLR2 ؊/؊ ) developed a more severe colitis than wild-type mice in the dextran sodium sulfate (DSS) model. However, they had significantly fewer eosinophils in the submucosa of the cecum (P < 0.01) and mid-colon (P < 0.01) than did wild-type mice after DSS treatment. Decreased eosinophilia in TLR2 ؊/؊ mice was associated with lower levels of cecal CCL11 (P < 0.01). Peritoneal eosinophils did not express TLR2 protein, but TLR2 ligand injection into the peritoneal cavity induced local eosinophil recruitment, indicating that TLR2 activation of other cell types can mediate eosinophil recruitment. After DSS treatment, mast celldeficient (Kit W-sh/W-sh ) mice had similar levels of intestinal tissue eosinophilia were observed as those in wild-type mice. However, mast cell-deficient mice were partially protected from DSS-induced weight loss, an effect that was reversed by mast cell reconstitution. Overall, this study indicates a critical role for indirect TLR2-dependent pathways, but not mast cells, in the generation of eosinophilia in the large intestine during experimental colitis and has important implications for the regulation of eosinophils at mucosal inflammatory sites.

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Enhanced histamine metabolism: a comparative analysis of collagenous colitis and food allergy with respect to the role of diet and NSAID use

Schwab¹,

Hahn²,

Raithel³

2003

Inflammation Research

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Objectives and Design: To compare clinical data and histamine metabolism of patients with collagenous colitis with those of food allergy. Methods: In 17 patients with collagenous colitis, clinical findings (diarrhoea, abdominal pain) were recorded. Plasma (for histamine) and 12-h-urine (for histamine and n-methylhistamine, all measured by RIA) were collected during two days with an unrestricted diet followed by two days with an hypoallergenic. The clinical data and measured values were compared with those from patients with confirmed food allergy (n = 21) and controls (n = 41). Results: Patients with collagenous colitis were found to present with significantly more liquid stools than patients with food allergy (p < 0.001) during both types of diet, but they did not experience more abdominal pain. N-methylhistamine in 12-h-urine was significantly increased during both types of diet in patients with collagenous colitis and food allergy when compared with controls (p < 0.001 for all). Patients with food allergy -but not those with collagenous colitisshowed a significant decrease of severity of pain (p < 0.05) when the diet was changed to the elimination protocol. Conclusion: Histamine is extensively produced and metabolised in patients with collagenous colitis. In contrast to food allergy, the allergenic potency of the administered food seems not to influence histamine production in collagenous colitis. However, histamine metabolism corresponds with the clinical activity in both patients with food allergy and collagenous colitis.

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Distribution of mast cells, macrophages of colonic mucosa of patients with collagenous colitis and inflammatory bowel disease

Cited by 42 publications

References 0 publications

Essential role for mast cell tryptase in acute experimental colitis

Essential role for mast cell tryptase in acute experimental colitis

Tissue Eosinophilia in a Mouse Model of Colitis Is Highly Dependent on TLR2 and Independent of Mast Cells

Enhanced histamine metabolism: a comparative analysis of collagenous colitis and food allergy with respect to the role of diet and NSAID use

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