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Background  Helminthiasis and tuberculosis (TB) coincide geographically and there is much interest in exploring how concurrent worm infections might alter immune responses against bacilli and might necessitate altered therapeutic approaches. A DNA vaccine that codifies heat shock protein Hsp65 from  M. leprae  (DNAhsp65) has been used in therapy during experimental tuberculosis. This study focused on the impact of the co-existence of worms and TB on the therapeutic effects of DNAhsp65.    Methodology/Principal Findings  Mice were infected with  Toxocara canis  or with  Schistosoma mansoni , followed by coinfection with  M. tuberculosis  and treatment with DNAhsp65. While  T. canis  infection did not increase vulnerability to pulmonary TB,  S. mansoni  enhanced susceptibility to TB as shown by higher numbers of bacteria in the lungs and spleen, which was associated with an increase in Th2 and regulatory cytokines. However, in coinfected mice, the therapeutic effect of DNAhsp65 was not abrogated, as indicated by colony forming units and analysis of histopathological changes.  In vitro  studies indicated that Hsp65-specific IFN-γ production was correlated with vaccine-induced protection in coinfected mice. Moreover, in  S. mansoni -coinfected mice, DNA treatment inhibited  in vivo  TGF-β and IL-10 production, which could be associated with long-term protection.    Conclusions/Significance  We have demonstrated that the therapeutic effects of DNAhsp65 in experimental TB infection are persistent in the presence of an unrelated Th2 immune response induced by helminth infections.

Helminth Coinfection Does Not Affect Therapeutic Effect of a DNA Vaccine in Mice Harboring Tuberculosis