Macrophages in Tuberculosis

Tuberculosis (TB)

TB is a chronic inflammatory disease caused by a Mycobacterium tuberculosis (Mtb) infection. TB typically is a disease of the lung, which serves both as a port of entry and as the major site of disease outbreaks. This is followed by an early inflammatory response, induced by both bacterial and host factors, which results in the recruitment of leukocytes from neighboring blood vessels to the site of infection. Subversion of the death modality of macrophages, the principal host cells infected by TB, is a common feature of several other intracellular pathogens. Various bacteria and intracellular parasites induce apoptosis or necrosis following infection. While antimycobacterial therapy exists, currently available drugs are only partially effective because of the impermeable nature of the mycobacterial cell wall and the propensity of Mtb to develop resistance. One additional problem is that Mtb has the capacity to remain viable within infected hosts for a prolonged time.

Role of Macrophages in TB

Infection of a host with Mtb is initiated following the inhalation of droplets (aerosols) containing a small number of bacilli. In the early stage of Mtb infection, macrophages show pro-inflammatory responses like M1 macrophages contributing to the restriction of Mtb survival (Mtb-infected M1 macrophages are transformed into M2 macrophages with suppressive activities in their antibacterial responses over time). Alveolar macrophages can effectively phagocytize and transfer the phagocytosed Mtb to the destructive environment of lysosomes. However, some bacilli can escape from the lysosome and survive within the macrophage. These macrophages harbor the pathogen and transport it to draining lymph nodes. A small granulomatous lesion develops containing the bacteria. Mtb-infected macrophages can differentiate into foamy macrophages by the accumulation of lipid, which are hallmarks of TB lesions. When foamy macrophages leave the original granuloma to promote the dissemination, giving the bacteria access to nearby airways and thus the ability to spread within the lung and elsewhere within the body. Thus, Mtb-infected alveolar. In the case of immunodeficiency, for example, when T cell function is compromised, unrestricted growth and necrosis within macrophages cause dissemination of tubercle bacilli.

Generation of Mtb-infected foamy macrophages during the formation of TB granulomas. Fig.1 Generation of Mtb-infected foamy macrophages during the formation of TB granulomas. (Shim, 2020)

Strategies to Conquer Macrophages

Therapies Targeting macrophages in TB

Host-directed therapy (HDT) against Mycobacterium tuberculosis. Fig.2 Host-directed therapy (HDT) against Mycobacterium tuberculosis. (Ahmed, 2020)

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References

  1. Shim, D.; et al. Mycobacterium tuberculosis infection-driven foamy macrophages and their implications in tuberculosis control as targets for host-directed therapy. Front Immunol. 2020, 11: 910.
  2. Ahmed, S.; et al. Host-directed therapy as a novel treatment strategy to overcome tuberculosis: targeting immune modulation. Antibiotics (Basel). 2020, 9(1):21-.
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