Abstract

Abstract Epidemiological data suggest protection from allergic diseases when exposed to infectious agents during early stages of life. As allergies are mainly characterized as an unchecked Th2 response, modulation of the immune responses by pathogens have been considered to be a major factor in mediating the protection. Recent evidences implicate a key role staged by immuno-regulatory mechanisms induced upon infection in ameliorating these allergic disorders. A longitudinal study had demonstrated the reduced frequency and incidence of asthma in children, who had a prior infection from Salmonella typhi. A subsequent investigation demonstrated reduced airway inflammation in mice infected with Salmonella; however the mechanism still remained obscure. In this study, we aimed to delineate the potential mechanisms induced upon Salmonella typhimurium infection which resulted in the amelioration of allergic airway inflammation in mice. We report a significant increase in CD11b+ Gr1+ myeloid cell population in those mice that had been infected with Salmonella. Using in vitro and in vivo analysis we suggest that these myeloid cells could potentially ameliorate airway inflammation by affecting the stability of Th2 cells. In contrast to our initial hypothesis, regulatory T cells were not involved in the protective effect of salmonella infection.

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