Abstract

Mycobacterium bovis Bacillus Calmette-Guérin (BCG) vaccination has been shown to inhibit allergic airway inflammation in animal models, associated with the regulation of allergen-specific T-cell immunity. However, little is known about whether neonatal BCG treatment could inhibit allergic inflammation by regulating allergen-specific T-cell response in aged mice. This study was aimed to investigate the impact of neonatal BCG treatment on allergic asthma and possible mechanism(s) underlying the action of BCG in different ages of mice. C57BL/6 neonates were vaccinated with BCG on days 1, 7 and 14, sensitized with ovalbumin (OVA) at 5 and 7 weeks of age, and then challenged with allergen at 9 or 45 weeks of age for early- or late-challenged asthma. Their airway inflammation and allergen-specific T-cell responses were characterized. Following early-challenge, BCG vaccination inhibited airway hyper-responsiveness (AHR), infiltration of eosinophils and mucous overproduction (P < 0.05), and shifted OVA-specific predominant Th2- to Th1-type cytokine responses in both the bronchoalveolar lavage fluid and the splenocyte supernatants (P < 0.05). In late-challenged mice, neonatal BCG treatment attenuated AHR and eosinophilia (P < 0.05), but failed to modulate allergen-specific cytokine responses. Our data suggest that neonatal BCG vaccination has a long-term effect on inhibiting AHR and eosinophilia, which is associated with the modulation of Th1/Th2 cytokine production in early-, but not in late-challenged mice. Thus, different mechanisms may mediate the long-term protective effect of BCG neonatal vaccination differently in younger adult and aged mice.

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