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BioMed Research International
Volume 2017, Article ID 8796760, 8 pages
Research Article

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

1Unidad Académica de Ciencias Biológicas, Laboratorio de Bioquímica Molecular e Inmunobiologia, Universidad Autónoma de Zacatecas, Av. Preparatoria S/N. Col. Agronómicas, 98066 Zacatecas, ZAC, Mexico
2Catedra-CONACYT, Avenida Insurgentes Sur 1685, Guadalupe Inn, 01020 Álvaro Obregón, CDMX, Mexico

Correspondence should be addressed to G. G. Guerrero; moc.liamg@9orerreugolg

Received 16 March 2017; Revised 13 June 2017; Accepted 22 June 2017; Published 27 September 2017

Academic Editor: Subash Babu

Copyright © 2017 C. E. Rivas-Santiago and G. G. Guerrero. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 M. tuberculosis 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 Mycobacterium bovis Bacillus Calmette Güerin (BCG) vaccinated mice protected adult mice from intradermal M. lepraemurium infection and a difference in iNOS was observed. In the present work, we have found that intramuscular IFN-α boosting of Mycobacterium bovis Bacillus Calmette Güerin (BCG) vaccine, either in vitro (human cell line or macrophages derived from PBMC) or in vivo (aerosol mouse model of MTb infection), promoted mostly the development of specific anti-antimycobacterial Th1 type cytokines (IFN-γ; IL-12, TNF-alpha, and IL-17; IL1β) 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 M. tuberculosis infection.