Mast cells are not essential to inflammation in murine model of colitis

Chin, Kenley W.; Barrett, Kim E.

doi:10.1007/bf02088336

Cited by 37 publications

(27 citation statements)

References 12 publications

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“…However, the role of mast cells in this model is controversial and contradictory (16,17). In this study, we present a consistent novel chemically induced immunological model for colonic IBD associated with mast cell activation.…”

Section: Nflammatory Bowel Disease (Ibd)mentioning

confidence: 94%

Critical Role for Mast Cells in the Pathogenesis of 2,4-Dinitrobenzene-Induced Murine Colonic Hypersensitivity Reaction

Rijnierse

Koster

Nijkamp

et al. 2006

The Journal of Immunology

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The immunological mechanisms underlying the role of mast cells in the pathogenesis of inflammatory bowel disease (IBD) are poorly defined. In this study, non-IgE mediated colonic hypersensitivity responses in BALB/c mice induced by skin sensitization with dinitrofluorobenzene (DNFB) followed by an intrarectal challenge with dinitrobenzene sulfonic acid featured as a model to study the role of mast cells in the development of IBD. Vehicle- or DNFB-sensitized mice were monitored for clinical symptoms and inflammation 72 h after dinitrobenzene sulfonic acid challenge. DNFB-sensitized mice developed diarrheic stool, increased colonic vascular permeability, hypertrophy of colonic lymphoid follicles (colonic patches), and showed cellular infiltration at the microscopic level. Increased numbers of mast cells were found in the colon of DNFB-sensitized mice located in and around colonic patches associated with elevated levels of mouse mast cell protease-1 in plasma indicating mast cell activation. Colonic patches of DNFB mice, stimulated in vitro with stem cell factor indicated that an increase in TNF-α levels in the colon is mainly mast cell originated. Finally, neutrophil infiltration was observed in the colon of DNFB-sensitized mice. Induction of this model in mast cell-deficient WBB6F1 W/Wv mice shows a profound reduction of characteristics of the colonic hypersensitivity reaction. Reconstitution with bone marrow-derived mast cells in WBB6F1 W/Wv mice fully restored the inflammatory response. This study demonstrates the importance of mast cells in the development of clinical symptoms and inflammation in the presented murine model for IBD.

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Section: Nflammatory Bowel Disease (Ibd)mentioning

confidence: 94%

Critical Role for Mast Cells in the Pathogenesis of 2,4-Dinitrobenzene-Induced Murine Colonic Hypersensitivity Reaction

Rijnierse

Koster

Nijkamp

et al. 2006

The Journal of Immunology

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“…Each colon received a macroscopic score (from 0 to 10) by two independent blinded observers as described by Chin et al (39). For histologic score, colon sections were stained with H&E and scored as follows: 0, no inflammation; 1, low leukocyte infiltration; 2, moderate leukocyte infiltration; 3, high infiltration, moderate fibrosis and goblet loss; and 4, massive loss of goblet cells, extensive fibrosis, and thickening of the colon wall.…”

Section: Assessment Of Inflammationmentioning

confidence: 99%

The Proinflammatory Effect of Prostaglandin E2 in Experimental Inflammatory Bowel Disease Is Mediated through the IL-23→IL-17 Axis

Sheibanie

Yen

Khayrullina

et al. 2007

The Journal of Immunology

252

196

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Although Crohn’s disease has been traditionally considered to be Th1-mediated, the newly identified Th17 cells emerged recently as crucial participants. Th1/Th17 differentiation is controlled primarily by the IL-12 family of cytokines secreted by activated dendritic cells (DCs) and macrophages. IL-23 and IL-12/IL-27 have opposite effects, supporting the Th17 and Th1 phenotypes, respectively. We found that PGE2, a major lipid mediator released in inflammatory conditions, shifts the IL-12/IL-23 balance in DCs in favor of IL-23, and propose that high levels of PGE2 exacerbate the inflammatory process in inflammatory bowel disease through the IL-23→IL-17 axis. We assessed the effects of PGE2 on IL-12, IL-27, and IL-23 and found that PGE2 promotes IL-23, inhibits IL-12 and IL-27 expression and release from stimulated DCs, and subsequently induces IL-17 production in activated T cells. The effects of PGE2 are mediated through the EP2/EP4 receptors on DCs. In vivo, we assessed the effects of PGE analogs in an experimental model for inflammatory bowel disease and found that the exacerbation of clinical symptoms and histopathology correlated with an increase in IL-23 and IL-17, a decrease in IL-12p35 expression in colon and mesenteric lymph nodes, and a substantial increase in the number of infiltrating neutrophils and of CD4+IL-17+ T cells in the colonic tissue. These studies suggest that high levels of PGE2 exacerbate the inflammatory process through the preferential expression and release of DC-derived IL-23 and the subsequent support of the autoreactive/inflammatory Th17 phenotype.

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“…This model results in a transmural inflammatory response that does not resolve within 7 days but develops from an acute to a chronic form of inflammation. Mast cell hyperplasia and infiltration of lymphocytes has been noted for at least 2 weeks postadministration [23,24]. Mice were killed 3 or 7 days after colitis induction.…”

Section: Trinitrobenzene Sulfonic Acid (Tnbs)-induced Colitismentioning

confidence: 99%

“…Groups of mice were killed by cervical dislocation, the colon excised, and the severity of colonic damage assessed using the criteria previously described for the acetic acid-induced colitis [22] or for the TNBS-induced colitis [23]. These scoring systems include features of clinical colitis, macroscopically visible damage, the presence and severity of adhesions, the presence of diarrhea (for these purposes diarrhea was defined as loose, watery stool), and maximal bowel wall thickness (mm) and are shown in Tables 1 and 2.…”

Section: Assessment Of Severity Of Colitismentioning

confidence: 99%

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

McCafferty

Smith

Granger

et al. 1999

Journal of Leukocyte Biology

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Biopsy specimens from patients with inflammatory bowel disease have demonstrated an up-regulation of P-selectin, suggesting a role for P-selectin in intestinal inflammation. We examined the role of P-selectin in experimental intestinal inflammation using mice deficient in P-selectin alone or in combination with either ICAM-1 or E-selectin. Colitis was induced using acetic acid or trinitrobenzene sulfonic acid (TNBS). Damage scores and neutrophil infiltration 24 h post acetic acid were not different between wild-type and P-selectin-or P-selectin/ICAM-1-deficient mice, whereas P/E-selectin-deficient mice had enhanced leukocyte recruitment and damage. At 72 h an attenuation in damage scores and a slight decrease in neutrophil infiltration was observed in the P-and P/ICAM-deficient animals. The P/E-selectin-deficient mice maintained enhanced leukocyte recruitment and damage. In wild-type mice P-selectin expression was elevated 48 and 72 h post acetic acid-induced inflammation. Surprisingly, P-selectin or P-selectin/ICAM-1 deficiency did not improve the inflammation induced by TNBS over 7 days. In fact, increased mortality was observed. Antiadhesion therapy may play only a limited, beneficial role and often a detrimental role in intestinal inflammation. J. Leukoc. Biol. 66: 67-74; 1999.

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Mast cells are not essential to inflammation in murine model of colitis

Cited by 37 publications

References 12 publications

Critical Role for Mast Cells in the Pathogenesis of 2,4-Dinitrobenzene-Induced Murine Colonic Hypersensitivity Reaction

Critical Role for Mast Cells in the Pathogenesis of 2,4-Dinitrobenzene-Induced Murine Colonic Hypersensitivity Reaction

The Proinflammatory Effect of Prostaglandin E2 in Experimental Inflammatory Bowel Disease Is Mediated through the IL-23→IL-17 Axis

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

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