Clinical isolates of Mycobacterium tuberculosis in Argentina differentially induces respiratory burst via TLR2 and dectin-1 in neutrophils as possible mechanism of immune escape.

MARÍA MERCEDES ROMERO; JUAN IGNACIO BASILE; BEATRIZ LOPEZ; VIVIANA RITACCO; LUCÍA BARRERA; M.C. SASIAIN; ALEMAN MERCEDES

Milan

Congreso; 15th International Congress of Immunology ? ICI.; 2013

Tuberculosis (TB) remains a major global health problem caused by inhalation of aerosols containing Mycobacterium tuberculosis (Mtb). Neutrophils (PMN) play a protective role in TB by inducing apoptosis through the generation of oxygen intermediates (ROS), a mechanism which allows removal of infected PMN, thereby limiting the infection. Bacterial factors can influence these early stages of infection. Previously, we found that a highly epidemic multidrug-resistant Mtb strain of the Haarlem family induces lower ROS production and apoptosis in PMN than a less spread multidrug-resistant strain of the LAM family. The present study was designed to test the hypothesis that such differences in Mtb interaction with the innate immune system would be related to differences in bacterial wall composition