Mycobacterial infection inhibits established allergic inflammatory responses via alteration of cytokine production and vascular cell adhesion molecule-1 expression

Authors

  • Xi Yang,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Yijun Fan,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Shuhe Wang,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Xiaobing Han,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Jie Yang,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Laura Bilenki,

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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  • Lijun Chen

    1. Immune Regulation of Allergy Research Group, Departments of Medical Microbiology and Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
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Dr Xi Yang, Department of Medical Microbiology, University of Manitoba, Room 523, 730 William Avenue, Winnipeg, Manitoba, Canada R3E OW3. E-mail: yangxi@cc.umanitoba.ca

Summary

Our previous studies, as well as those of others, have demonstrated that local or systemic Mycobacterium bovis bacille Calmette–Gue´rin (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.

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