Increased Expression of Intercellular Adhesion Molecule-1 and Mucosal Adhesion Molecule α4β7 Integrin in Small Intestinal Mucosa of Adult Patients with Food Allergy

Veres, Gábor; Helin, Timo; Arató, András; Färkkilä, Martti; Kantele, A.; Suomalainen, Hanna; Savilahti, Erkki

doi:10.1006/clim.2001.5032

Cited by 20 publications

(10 citation statements)

References 27 publications

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“…Leukocyte recruitment into the GI tract and gut-associated lymphoid tissue are thought to be critically regulated by ␤ 7integrin [31,32,59,60]. Indeed, the expression of MAdCAM-1 and ␣ 4 ␤ 7 expression on leukocytes in the intestinal mucosa is up-regulated significantly in GI diseases, including cows milk allergy and food allergy [61,62]. Recently, experimental stud- ies have demonstrated that leukocyte recruitment into the large intestine can occur in a ␤ 7 -integrin-independent manner [32,33,60].…”

Section: Discussionmentioning

confidence: 99%

ICAM-1-dependent pathways regulate colonic eosinophilic inflammation

Forbes

Hulett

Ahrens

et al. 2006

Journal of Leukocyte Biology

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Eosinophilic inflammation is a common feature of numerous eosinophil-associated gastrointestinal (EGID) diseases. Central to eosinophil migration into the gastrointestinal tract are the integrin-mediated interactions with adhesion molecules. Although the mechanisms regulating eosinophil homing into the small intestine have begun to be elucidated, the adhesion pathways responsible for eosinophil trafficking into the large intestine are unknown. We investigated the role of adhesion pathways in eosinophil recruitment into the large intestine during homeostasis and disease. First, using a hapten-induced colonic injury model, we demonstrate that in contrast to the small intestine, eosinophil recruitment into the colon is regulated by a beta7 -integrin addressin cell adhesion molecule-1-independent pathway. Characterization of integrin expression on colonic eosinophils by flow cytometry analysis revealed that colonic CC chemokine receptor 3+ eosinophils express the intercellular adhesion molecule-1 (ICAM-1) counter-receptor integrins alphaL, alphaM, and beta2. Using ICAM-1-deficient mice and anti-ICAM-1 neutralizing antibodies, we show that hapten-induced colonic eosinophilic inflammation is critically dependent on ICAM-1. These studies demonstrate that beta2 -integrin/ICAM-1-dependent pathways are integral to eosinophil recruitment into the colon during GI inflammation associated with colonic injury.

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Section: Discussionmentioning

confidence: 99%

ICAM-1-dependent pathways regulate colonic eosinophilic inflammation

Forbes

Hulett

Ahrens

et al. 2006

Journal of Leukocyte Biology

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“…On the other hand, we did not find evidence that either ICAM-1 or VCAM-1 is involved in T lymphocyte migration in the small intestine. Several studies (7,11,33) on food allergy and animal models have suggested that the increased expression of ICAM-1 or VCAM-1 is related to the pathogenesis of leukocyte infiltration to the intestinal mucosa. We surmise that leukocyte subpopulations other than T cells, such as neutrophils, might play important roles via an ICAM-1-dependent mechanism in these situations.…”

Section: Discussionmentioning

confidence: 99%

“…Studies of other atopic diseases and animal models suggest that adhesion molecules and mucosal lymphocytes are implicated in the pathogenesis of food allergy (12). Several clinical reports (7,33) have also indicated that the expression of adhesion molecules is increased in the duodenal mucosa of adult patients with food allergies or of infants with cow's milk-sensitive enteropathy. However, only a few studies have addressed lymphocyte trafficking in food allergies, and the mechanisms of directly "trafficking" cells have only scarcely been explored (11,28).…”

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confidence: 99%

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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“…Dans un modèle d'allergie alimentaire chez la souris, les récepteurs CCR8 et les ligands de CCR4, CCL17 et CCL22 sont surexprimés au niveau du tube digestif [57]. Chez des patients allergiques aux céréales (blé, avoine, seigle) ou au lait, l'expression de ICAM-1 et de ␣4␤7 se retrouve augmentée dans la lamina propria [58]. Enfin, on retrouve encore une fois l'implication du récepteur de chimiokine CX3CR1 dans l'allergie alimentaire.…”

Section: Les Récepteurs De Chimiokines Dans L'allergie Alimentaireunclassified