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Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment

Authors
  • Gouveia, Ana Cláudia Carvalho1
  • Brugiolo, Alessa Sin Singer1
  • Alves, Caio César Souza1
  • Silva, Flávia Márcia Castro1
  • Mesquita, Felipe Pereira1
  • Gameiro, Jacy1
  • Ferreira, Ana Paula1
  • 1 Universidade Federal de Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil , Juiz de Fora (Brazil)
Type
Published Article
Journal
Journal of Clinical Immunology
Publisher
Springer-Verlag
Publication Date
Aug 04, 2012
Volume
33
Issue
1
Pages
235–245
Identifiers
DOI: 10.1007/s10875-012-9746-4
Source
Springer Nature
Keywords
License
Yellow

Abstract

ObjectiveThis study aimed to determine whether Mycobacterium bovis Bacillus Calmette-Guérin (BCG) treatment can reverse an established allergic airway inflammation in a BALB/c mouse model of ovalbumin (OVA)-induced airway inflammation.MethodsOVA sensitized BALB/c mice were challenged with aerosolized OVA on days 28 to 30, 34, 41 and 63. Mice were intranasal treated with BCG on days 35 and 42. Twenty-four hours after the last challenge, blood samples were collected to detect anti-OVA immunoglobulin isotypes, and bronchoalveolar lavage (BAL) was harvested for cell count. Additionally, lungs were collected for histological analysis, detection of the eosinophil peroxidase (EPO) activity and measurement of cytokines and CCL11. The expression of CTLA-4, Foxp3 and IL-10 was also determined in lung tissue by flow cytometry.ResultsBCG treatment was able to inhibit an established allergic Th2-response, by decreasing the allergen-induced eosinophilic inflammation, EPO activity, levels of CCL11 and IL-4, serum levels of IgE and IgG1. Mycobacteria treatment increased lung levels of IFN-γ, IL-10 and TGF-β, and expressions of Foxp3 and CTLA-4 in CD4+T cells. Additionally, an increased production of IL-10 by CD8+ T cells was observed, even though no detectable changes in CD4+IL-10+ was noticed.ConclusionBCG treatment inhibits features of allergic airway inflammation and the results suggest that the mechanism underlying the down-regulatory effects of BCG on OVA-induced airway inflammation appear to be associated with the induction of both Th1 and T regulatory immune responses.

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