Spatial heterogeneity of TNF-α-induced T cell migration  to colonic mucosa is mediated by MAdCAM-1 and VCAM-1

Watanabe, Chikako; Miura, Soichiro; Hokari, Ryota; Teramoto, Ken; Ogino, Takashi; Komoto, Shunsuke; Hara, Yuriko; Koseki, Seiichiro; Tsuzuki, Yoshikazu; Nagata, Hiroshi; Granger, D. Neil; Ishii, Hiromasa

doi:10.1152/ajpgi.00026.2002

Cited by 39 publications

(36 citation statements)

References 30 publications

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“…TNF-␣ produced from mast cells might be an important factor for the upregulation of adhesion molecules including MAdCAM-1 (16,35). To our knowledge, this is the first direct demonstration of lymphocyte migration to gut-associated lymphoid organs and intestinal mucosal microvessels in situ in a chronic food allergy model.…”

Section: Discussionmentioning

confidence: 66%

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

Ogawa

Miura²,

Tsuzuki³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1. Am J Physiol Gastrointest Liver Physiol 286: G702-G710, 2004. First published December 11, 2003 10.1152/ajpgi.00183.2003.-Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.Brown Norway rats; rat mast cell protease II; delayed type hypersensitivity; Peyer's patch; intercellular adhesion molecule-1 THE CLINICAL MANIFESTATIONS of allergic reactions from food intolerance may be localized to the gut, including abdominal discomfort, nausea, vomiting, and diarrhea. Type I or IgEmediated allergic reactions are involved in early-phase symptoms of food allergy (6,8). On the other hand, cell-mediated reactions are also involved in the late phase and symptoms are often prolonged, causing mucosal damage such as crypt hyperplasia, villus atrophy, and lymphocyte infiltration (11,13,27,30). Because human research is restricted, animal models of food allergies would be of significant value. Several efforts have been made to develop rodent models of food allergy (10,14,32). However, few models have been validated for studying the effects of chronic antigen exposure or for relevance to clinical situations involving both IgE-and cell-mediated reactions (21,22,28). Although several groups (10) have investigated the effect of repeated oral challenge in rats with IgEmediated hypersensitivity, lymphocyte infiltration was not obvious in the intestinal mucosa of these animals. Only a recent report by Yang et al. (36) has demonstrated that the oral antigen challenge of sensitized Sprague-Dawley rats induces sustained epithelial dysfunction with inflammator...

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Section: Discussionmentioning

confidence: 66%

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

Ogawa

Miura²,

Tsuzuki³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The microcirculation of colonic mucosa was also observed from the mucosal surface, and lymphocyte migration was observed through a fluorescence microscope as previously described (28). The lymphocytes staying Ͼ30 s in mucosal microvessels were defined as sticking lymphocytes.…”

Section: Separation Of Lpls and Iels From Mouse Intestinementioning

confidence: 99%

Demonstration of functional role of TECK/CCL25 in T lymphocyte-endothelium interaction in inflamed and uninflamed intestinal mucosa

Hosoe¹,

Miura²,

Watanabe³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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It has recently been suggested that C-C chemokines may play a role in the organ-specific homing of lymphocytes, but there is not enough in vivo evidence in intestinal mucosa. The aim of this study was to examine whether thymus-expressed chemokine (TECK)/CCL25 and its ligand CCR9 are involved in T-lymphocyte interaction with microvessels of murine intestinal mucosa. T lymphocytes from the small intestine were fluorescence labeled, and their adhesion to mucosal microvessels was observed by intravital microscopy. Lamina proprial lymphocytes (LPL) and intraepithelial lymphocytes (IEL) adhered to both the small intestine and colon, and desensitization of CCR9 with TECK/CCL25 or anti-TECK/CCL25 antibody significantly inhibited these adhesions only in small intestine. At both sites, TNF-α significantly increased LPL adhesion but not IEL adhesion. Desensitization of CCR9 or anti-TECK/CCL25 antibody also attenuated the TNF-α-induced LPL adhesion in the small intestine. Increased expression of TECK/CCL25 by TNF-α was observed in the lamina propria of small intestine. TECK/CCL25 may thus play an important role in the adherence of mucosal lymphocytes to the microvessels of the small intestine but not the colon under uninflamed as well as inflamed conditions.

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“…There are indeed several reports indicating that antibodies against other adhesion molecules (ICAM-1 or VCAM-1) attenuate the increased leucocyte adhesion in intestinal venules [7,18,19]. In the case of ICAM-1, however, we have already reported that up-regulated ICAM-1 is not involved in T lymphocyte-endothelial adhesion in the inflamed colon [15]. Moreover, in the case of VCAM-1, most of the reports have given results obtained from a relatively acute course of inflammation, so we speculate that especially in the case of chronic colitis, MAdCAM-1, rather than VCAM-1 or ICAM-1, may play a key role in T and B lymphocyte migration.…”

Section: Discussionmentioning

confidence: 70%

“…[14]. The cells were resuspended in 0·2 ml of the medium and used within 30 min The microcirculation in the colonic mucosa was observed from the mucosal surface with an inverted-type fluorescence microscope (Diaphot TMD-2S, Nikon, Tokyo) equipped with a silicon intensifier target (SIT) image tube camera (C-2400-08, Hamamatsu Photonics Co., Shizuoka, Japan) as previously reported [15]. Lymphocytes (3 ¥ 10 7 dissolved in 0·3 ml) were injected into tail veins of the recipient mice for 5 min.…”

Section: Administration Of Dss and Assessment Of Colonic Inflammationmentioning

confidence: 99%

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Increased lymphocyte trafficking to colonic microvessels is dependent on MAdCAM-1 and C-C chemokine mLARC/CCL20 in DSS-induced mice colitis

Teramoto

Miura

Tsuzuki

et al. 2005

Clinical and Experimental Immunology

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SummaryAlthough enhanced lymphocyte trafficking is associated with colitis formation, little information about its regulation is available. The aim of this study was to examine how the murine liver and activation-regulated chemokine (mLARC/CCL20) contributes to lymphocyte recruitment in concert with vascular adhesion molecules in murine chronic experimental colitis. T and B lymphocytes isolated from the spleen were fluorescence-labelled and administered to recipient mice. Lymphocyte adhesion to microvessels of the colonic mucosa and submucosa was observed with an intravital microscope. To induce colitis, the mice received two cycles of treatment with 2% dextran sodium sulphate (DSS). In some of the experiments antibodies against the adhesion molecules or anti-mLARC/CCL20 were administered, or CC chemokine receptor 6 (CCR6) of the lymphocytes was desensitized with excess amounts of mLARC/CCL20. Significant increases in T and B cell adhesion to the microvessels of the DSS-treated mucosa and submucosa were observed. In chronic colitis, the accumulation of lymphocytes was significantly inhibited by anti-mucosal addressin cell adhesion molecule (MAdCAM)-1 mAb, but not by anti-vascular cell adhesion molecule-1. In DSS-treated colonic tissue, the expression of mLARC/CCL20 was significantly increased, the blocking of mLARC/CCL20 by monoclonal antibody or the desensitization of CCR6 with mLARC/CCL20 significantly attenuated the DSS-induced T and B cell accumulation. However, the combination of blocking CCR6 with MAdCAM-1 did not further inhibit these accumulations. These results suggest that in chronic DSS-induced colitis, both MAdCAM-1 and mLARC/CCL20 may play important roles in T and B lymphocyte adhesion in the inflamed colon under flow conditions.

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Spatial heterogeneity of TNF-α-induced T cell migration to colonic mucosa is mediated by MAdCAM-1 and VCAM-1

Cited by 39 publications

References 30 publications

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

Demonstration of functional role of TECK/CCL25 in T lymphocyte-endothelium interaction in inflamed and uninflamed intestinal mucosa

Increased lymphocyte trafficking to colonic microvessels is dependent on MAdCAM-1 and C-C chemokine mLARC/CCL20 in DSS-induced mice colitis

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