Gabriela Echeverria-Valencia

By Clara Espitia, Eden Rodríguez, Lucero Ramón-Luing, Gabriela Echeverría-Valencia and Antonio J. Vallecillo

Part of the book: Understanding Tuberculosis

By Gabriela Echeverria-Valencia, Susana Flores-Villalva and Clara I. Espitia

Virulence, is referred as the ability of a pathogen to cause disease, and for mycobacteria it depends on their ability to reside within host cells and evade the microbicidal mechanisms of macrophages. The outcome of tuberculosis (TB) infection is highly variable and it seems that the closest relationship between the Mycobacterium genre and humans has shaped the mycobacterial genome to encode bacterial factors that reflects a highly evolved and coordinated program of immune evasion strategies that interfere with both innate and adaptive immunity causing disease even in fully immunocompetent host. Although Mycobacterium tuberculosis (MTB) does not have classical virulence factors, it has described many virulence-associated genes and virulence lifestyle genes from Mycobacterium tuberculosis complex (MTBC). In this chapter, we describe the most important gene/molecule involved in the host defense modulation response, also the plethora of strategies to evade immune mechanisms of macrophage. We review the main genes whose inactivation in the mycobacterial genome leads to a measurable loss in virulence in the different validated TB models.

Part of the book: Mycobacterium

By Gabriela Echeverría-Valencia

Mycobacterium tuberculosis is the causal agent of human tuberculosis. The initial events of the establishment of the infection include the phagocytosis by several innate immune response cells. This chapter will discuss the immune cells involved, the phagocytic pattern recognition receptors (PPRs) that recognize and mediate bacteria phagocytosis (such as C-type lectin receptors, Toll-like receptors, complement receptors, and scavenger receptors), and the outcome of this initial interaction. Additionally, the bacterial strategies to evade the immune response—which includes the inhibition of the phagosome maturation and arresting of phagosome acidification, the mechanisms to survive to the reactive nitrogen species and reactive oxygen species, and finally, the resistance to the apoptosis and autophagy—will be reviewed. Finally, the host-pathogen interaction of M. tuberculosis with the phagocytic human cells during the primary events of the tuberculosis infection will also be reviewed.

Part of the book: Phagocytosis