Tuberculosis is a chronic bacterial infection that produces immunological abnormalities. In man and mice cell mediated immunity is essential for tuberculosis protection and it has been reported that Th17 cells and interleukin-17 contribute to protection, but they can also produce tissue damage by excessive recruitment of neutrophils.

The aim of this work is to define if IL-17 is related to protection or tissue damage using a murine model of progressive pulmonary tuberculosis.

Groups of BALB/c mice were infected with virulent Mycobacterium tuberculosis strain H37Rv. Mice were evaluated for survival, and lungs were collected at different days post-infection for microbiological, histopathological and immunological studies determining the IL-17 expression and local production by RT-PCR and immunohistochemistry respectively. In a second part of the study, infected mice were treated with neutralizing antibodies against IL-17 at different days post-infection during the pre-determined period of increased production of this cytokine. Lungs were collected at day 21 post-infection for the same studies mentioned above.

Infected lungs showed since the first day IL-17 production, essentially by airways epithelium and endothelium, at day 14 and 21positives cells were detected in the perivascular and peribronchial infiltrates and in granulomas. The gene expression kinetics showed the maximal IL-17 transcription at day 14 post-infection. In comparison with control animals, infected mice treated with IL-17neutralizing antibodies showed high bacilli burden and lesser inflammatory infiltrate.The production of IL-17 in these treated animals was reduced.

These results suggest that IL-17 is related to protection in this model of progressive pulmonary TB.