RNase7 but not psoriasin nor sPLA2-IIA associates to Mycobacterium tuberculosis during airway epithelial cells infection.

Tuberculosis (TB) is a disease caused by Mycobacterium tuberculosis (Mtb). Innate immunity is the first line of defense against Mtb and malfunctions in any of its components is associated with the susceptibility to the disease. Epithelial products, such as host defence peptides (HDP) are the first molecules produced to counteract the infection. Although a wide variety of HDP are produced by epithelial cells only few of them have been studied during Mtb infection. Here, we assessed the expression and production of the HDPs: psoriasin, sPLA2-IIA and RNase 7 in airway epithelial cells (NCI-H292), type II pneumocytes (A549 cells) and monocytes-derived macrophages from human peripheral blood mononuclear cells (bMDM) and from the human cell line THP1(MDM) after Mtb in vitro infection. Results show that psoriasin and sPLA2-IIA were not induced by Mtb in any of the evaluated cells, while RNase 7 was overexpressed in infected-airway epithelial cells. Intracellular analysis by flow cytometry demonstrated that the highest levels of RNase 7 were observed 6 h post-infection and the induction was dependent to direct interaction between airway epithelial cells and Mtb. Besides, analysis by electron microscopy show that RNase7 are capable to attach to cell-wall of intracellular mycobacteria. Our studies suggest that induction of RNase 7 in response to Mtb, could have a role in anti-mycobacterial immunity which need to be studied as an innate immune mechanism.

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