Macrophage plasticity as a therapeutic target in tuberculosis

Abstract

The macrophages contribute to host defense against intracellular pathogens such as mycobacteria. Mycobacteria interact with macrophages altering their polarization state, which propagates establishment of infection. Thus, molecular macrophage properties in mycobacterial infections are critical both for understanding the biology of the infections as well as identifying therapeutic targets. Here, we review recent advances in the understanding how altered macrophage polarization in mycobacterial infections may lead to the design of targeted therapies that may reprogram these macrophages for enhanced mycobactericidal function.

Plasma metabolomic analysis reveals the metabolic characteristics and potential diagnostic biomarkers of spinal tuberculosis

“…This ultimately reduces MTB -induced injury such as foamy macrophage formation, tuberculous granuloma, and caseous necrosis. Therefore, therapeutic strategies targeting the above links and MAPK [ 41 ] and GPCRs [ 42 , 43 ] may inhibit the reproduction and spread of MTB [ 44 ].…”

Expanded characterization of in vitro polarized M0, M1, and M2 human monocyte-derived macrophages: Bioenergetic and secreted mediator profiles

“…M2-like macrophages have wound-healing and inflammation-resolving capabilities, required to facilitate repair and resolution of inflammation. However, tumors and certain infections can create an environment favoring the wound-healing M2-like phenotype, which allows cancer and infection to progress [ 49 , 50 ]. Hence, repolarization or “re-educating” macrophages is an area of targeted therapy development.…”

Cell state transition analysis identifies interventions that improve control ofM. tuberculosisinfection by susceptible macrophages

“…Whether the IFN-I hyperactivity is a biomarker of a specific macrophage state (polarization phenotype) remains unknown. Delineating pathways that shape and maintain specific macrophage phenotypes causally linked to TB susceptibility should enable rational design of interventions to correct them and avoid drugs that cause non-specific immune suppression 28,29 .…”