title: Mycobacterial infection inhibits established allergic inflammatory responses via alteration of cytokine production and vascular cell adhesion molecule-1 expression.
abstract: Our previous studies, as well as those of others, have demonstrated that local or systemic Mycobacterium bovis bacille Calmette-Guérin (BCG) infection can inhibit de novo allergen-induced asthma-like reactions, but the effect of this infection on established allergic responses is unknown. The aim of this study was therefore to examine the effect of mycobacterial infection on established allergy in a murine model of asthma-like reaction. Mice were sensitized with ovalbumin (OVA) in alum followed by infection with BCG and subsequent intranasal challenge with the same allergen. In some experiments, mice were sensitized with OVA followed by intranasal challenge with OVA and then given BCG infection with subsequent rechallenge with OVA. Mice without BCG infection but treated with OVA in the same manner, were used as a control. The mice were examined for immunoglobulin E (IgE) response and eosinophilic inflammation, mucus production, cytokine/chemokine patterns and adhesion molecule expression in the lung. The results showed that postallergen BCG infection suppressed the established airway eosinophilia and mucus overproduction, but not IgE responses. The inhibition of asthma-like reactions by BCG infection was correlated with a shift of allergen-driven cytokine production pattern and, more interestingly, with a dramatic decrease of vascular cell adhesion molecule-1 (VCAM-1) expression in the lung. These findings suggest that intracellular bacterial infection can inhibit established allergic responses via alteration of local cytokine production and the expression of adhesion molecules.
authors.affiliation: Immune Regulation of Allergy Research Group, Department of Medical Microbiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. yangxi@cc.umanitoba.ca
authors.forename: Xi
authors.initials: X
authors.lastname: Yang
authors.forename: Yijun
authors.initials: Y
authors.lastname: Fan
authors.forename: Shuhe
authors.initials: S
authors.lastname: Wang
authors.forename: Xiaobing
authors.initials: X
authors.lastname: Han
authors.forename: Jie
authors.initials: J
authors.lastname: Yang
authors.forename: Laura
authors.initials: L
authors.lastname: Bilenki
authors.forename: Lijun
authors.initials: L
authors.lastname: Chen
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology; D001249:Asthma / Q000150:complications / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000276:immunology; D005260:Female; D007108:Immune Tolerance; D007073:Immunoglobulin E / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D009093:Mucus / Q000276:immunology; D009164:Mycobacterium Infections / Q000150:complications / Q000276:immunology*; D009163:Mycobacterium bovis; D010047:Ovalbumin / Q000276:immunology; D011657:Pulmonary Eosinophilia / Q000150:complications / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D000941:Antigens; D016207:Cytokines; D019010:Vascular Cell Adhesion Molecule-1; D007073:Immunoglobulin E; D010047:Ovalbumin