Host–Pathogen Interactions in Tuberculosis

Abstract

The development of massively parallel DNA sequencing is revealing the scale of mammalian bacterial colonization and suggests that Homo sapiens is colonized by between 103 and 104 bacterial phylotypes. The understanding of the complexity of host-bacterial interactions could explain why only a relatively tiny number of bacteria causing human diseases (Keijser et al., 2008; McKenna et al., 2008; Henderson et al., 2011). Over thousands of years microbes and mammals have co-evolve resulting in extraordinarily sophisticated molecular mechanism permitting the organism to survive together. Mycobacterium tuberculosis is one of the best examples of successful coevolution, since the bacilli have infected one third of the human population, but in 90% of the cases without causing overt disease (Bhowruth et al., 2008). The factors that regulate the course and outcome of infection by M. tuberculosis are multifaceted and involve a complex interplay between the immune system of the host and survival strategies employed by the bacilli (Mischenko et al., 2004). During the infection process and pathological development of human tuberculosis, M. tuberculosis expresses many molecules and recruits others from the host that allow the microorganism to recognize and be recognized by different host receptors. In this way, the knowledge of these interactions at the molecular level is of fundamental importance to understand all the events involved in entry, dissemination and persistence of the pathogenic mycobacteria and in the design of new highly specific therapeutic agents.