New insights into the interaction of Mycobacterium tuberculosis and human macrophages.
Mycobacterium tuberculosis is a facultative intracellular pathogen. It infects macrophages where it avoids elimination by interfering with host defense mechanisms. Until recently, it was assumed that the acidification of phagosomes is the major strategy of macrophages to eliminate M. tuberculosis. However, there is emerging evidence demonstrating that human macrophages are equipped with additional antimicrobial effector functions. Specifically, autophagy, efferocytosis and antimicrobial peptides have been identified as mechanisms to restrict mycobacterial proliferation. Here we review recent findings on effector functions of human macrophages and mechanisms of the pathogen to interfere with them.
Department of Internal Medicine 5 - Hematology/Oncology, University of Erlangen, Germany.
Heiko
H
Bruns
Steffen
S
Stenger
D023181:Antimicrobial Cationic Peptides / Q000235:genetics / Q000378:metabolism; D001343:Autophagy; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007109:Immunity; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology*; D009169:Mycobacterium tuberculosis / Q000502:physiology*; D010587:Phagocytosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D014376:Tuberculosis / Q000276:immunology* / Q000382:microbiology*; D014807:Vitamin D / Q000378:metabolism
D023181:Antimicrobial Cationic Peptides; D017382:Reactive Oxygen Species; D014807:Vitamin D