Macrophage Infection by Mycobacteria

Abstract

Mycobacterium tuberculosis is the etiological agent of tuberculosis. It is a pathogen that continues to draw international concerns particularly due to the emergence of multi-drug resistance and to the difficulties associated with the diagnosis and treatment of latent tuberculosis. A key process in the pathogenesis of this disease is the interaction between this pathogen and host macrophages. Invasion of the macrophages protects the pathogen from attack by the immune system, allows it to multiply while protected within the macrophages, and alters the immune response as it influences the profiles of the cytokine and chemokine responses. Key to the intracellular survival of the pathogen within the macrophages is the specific interaction between the pathogen and its virulence factors with the host. This review provides an a summary of pertinent literature on the topic of macrophage receptors utilized by the pathogen, its survival strategies within the macrophage, and the general profile of immune signalling upon exposure to the pathogen. The importance of specific macrophage receptors and certain components of the pathogen to the direction of the immune response are also discussed.

Investigating the Role of Everolimus in mTOR Inhibition and Autophagy Promotion as a Potential Host-Directed Therapeutic Target in Mycobacterium tuberculosis Infection

“…Then, the phagosome proceeds to fuse with the lysosome which further acidifies and degrades bacteria via enzymatic processes. However, Mtb alters the phagosome trafficking pathway through numerous methods, preventing its own elimination by this process [22,23]. Mtb uses phosphatidylinositol mannoside (PIM) to stimulate Rab14, promoting phagosome fusion with an early endosome, resulting in the prevention of phagosomal maturation and acidification [24].…”

Immunity to the Dual Threat of Silica Exposure and Mycobacterium tuberculosis

“…Alveolar macrophages represent the first line of defense against many airborne pathogens and inhaled environmental particles. The reaction of AMs after exposure to silica (70, 105–115) has been extensively studied. The tissue remodeling and formation of granulomas in response to exposure to both silica and Mtb suggest that similar mechanisms are involved in the elimination process in individuals exposed to silica or Mtb separately (116–118).…”

New antituberculosis drugs, regimens, and adjunct therapies: needs, advances, and future prospects

“…El TNF-α es la citocina que promueve la formación y mantenimiento de los granulomas, conteniendo al bacilo y previniendo su diseminación. Además, la secreción de TNF-α estimula la producción de RNS/ROS (vía complejos mitocondriales y la oxidasa NADH) e induce la apoptosis de las células infectadas (Philips and Ernst, 2012;Hossain and Norazmi, 2013;Saleh and Longhi, 2016;Peddireddy, Doddam and Ahmed, 2017).…”