IFN-<i>α</i> Boosting of<i> Mycobacterium bovis Bacillus</i> Calmette Güerin-Vaccine Promoted Th1 Type Cellular Response and Protection against<i> M. tuberculosis </i>Infection

Abstract

The role of type I IFNs in the pathogenesis and control of mycobacterial infection is still controversial. It has been reported that type I IFNs exacerbated <i>M. tuberculosis</i> infection through hampering Th1 type cellular immune response. However, under certain conditions they can act as natural immune adjuvants for commercial vaccines. At this point, we have reported recently that successive IFN-alpha boosting of <i>Mycobacterium bovis Bacillus Calmette Güerin</i> (BCG) vaccinated mice protected adult mice from intradermal <i>M. lepraemurium</i> infection and a difference in iNOS was observed. In the present work, we have found that intramuscular IFN-<i>α</i> boosting of <i>Mycobacterium bovis Bacillus Calmette Güerin</i> (BCG) vaccine, either in vitro (human cell line or macrophages derived from PBMC) or in vivo (aerosol mouse model of <i>MTb</i> infection), promoted mostly the development of specific anti-antimycobacterial Th1 type cytokines (IFN-<i>γ</i>; IL-12, TNF-alpha, and IL-17; IL1<i>β</i>) while bacterial load reduction (0.9 logs versus PBS or BCG vaccine) was observed. These findings indicate that, under the experimental settings reported here, interferon alpha can drive or affect the TH cellular immune response in favour of BCG-inducing immunity against <i>M. tuberculosis</i> infection.