The lungs of these treated animals showed significantly lower expression of TGF-β than control mice, suggesting that one of the factors related to necrosis was the suppression of TGF-β, which is a significant anti-inflammatory factor that participates in the control of excessive inflammation during late infection in this experimental model (Hernández-Pando et al., 2006) and human TB (Toossi and Ellner, 1998). This evidence concerns the gene TGFB1 and infection.