Interaction of Mycobacterium tuberculosis infected-epithelial alveolar cells with macrophages

Abstract

Tuberculosis (TB) is a chronic infectious disease, whose focus is primarily pulmonar, and is transmitted by the bacillus Mycobacterium tuberculosis. Type II alveolar epithelial cells (AEC-II) are among the first cells to come into contact with M. tuberculosis. The bacilli growth in AEC-II is faster than in alveolar macrophages, what makes epithelial cells propitious reservoirs to the development of the infection. AEC-II cells recognize M. tuberculosis constituents via pattern recognition receptors and get actived, secreting cytokines, chemokines, antimicrobial peptides, and surfactant proteins, which affect the microenvironment at the infection site and can regulate the response of resident lung leukocytes, such as macrophages. Thus, our aim is to determine whether infected AEC-II, through the release of proinflammatory cytokines, modulate macrophages polarization to a M1 profile, the plasticity of M2 macrophages, and the effector functions triggered by these cells. (AU)