Macrophage: A Cell With Many Faces and Functions in Tuberculosis
Mycobacterium tuberculosis (Mtb) is the causative agent of human tuberculosis (TB) which primarily infects the macrophages. Nearly a quarter of the world’s population is infected latently by Mtb. Only around 5%–10% of those infected develop active TB disease, particularly during suppressed host immu...
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Frontiers Media S.A.
2022-05-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2022.747799/full |
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author | Faraz Ahmad Anshu Rani Anwar Alam Sheeba Zarin Saurabh Pandey Hina Singh Seyed Ehtesham Hasnain Seyed Ehtesham Hasnain Nasreen Zafar Ehtesham |
author_facet | Faraz Ahmad Anshu Rani Anwar Alam Sheeba Zarin Saurabh Pandey Hina Singh Seyed Ehtesham Hasnain Seyed Ehtesham Hasnain Nasreen Zafar Ehtesham |
author_sort | Faraz Ahmad |
collection | DOAJ |
description | Mycobacterium tuberculosis (Mtb) is the causative agent of human tuberculosis (TB) which primarily infects the macrophages. Nearly a quarter of the world’s population is infected latently by Mtb. Only around 5%–10% of those infected develop active TB disease, particularly during suppressed host immune conditions or comorbidity such as HIV, hinting toward the heterogeneity of Mtb infection. The aerosolized Mtb first reaches the lungs, and the resident alveolar macrophages (AMs) are among the first cells to encounter the Mtb infection. Evidence suggests that early clearance of Mtb infection is associated with robust innate immune responses in resident macrophages. In addition to lung-resident macrophage subsets, the recruited monocytes and monocyte-derived macrophages (MDMs) have been suggested to have a protective role during Mtb infection. Mtb, by virtue of its unique cell surface lipids and secreted protein effectors, can evade killing by the innate immune cells and preferentially establish a niche within the AMs. Continuous efforts to delineate the determinants of host defense mechanisms have brought to the center stage the crucial role of macrophage phenotypical variations for functional adaptations in TB. The morphological and functional heterogeneity and plasticity of the macrophages aid in confining the dissemination of Mtb. However, during a suppressed or hyperactivated immune state, the Mtb virulence factors can affect macrophage homeostasis which may skew to favor pathogen growth, causing active TB. This mini-review is aimed at summarizing the interplay of Mtb pathomechanisms in the macrophages and the implications of macrophage heterogeneity and plasticity during Mtb infection. |
first_indexed | 2024-12-12T20:58:37Z |
format | Article |
id | doaj.art-1987a8700af242609eb269f71d5c7f90 |
institution | Directory Open Access Journal |
issn | 1664-3224 |
language | English |
last_indexed | 2024-12-12T20:58:37Z |
publishDate | 2022-05-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Immunology |
spelling | doaj.art-1987a8700af242609eb269f71d5c7f902022-12-22T00:12:13ZengFrontiers Media S.A.Frontiers in Immunology1664-32242022-05-011310.3389/fimmu.2022.747799747799Macrophage: A Cell With Many Faces and Functions in TuberculosisFaraz Ahmad0Anshu Rani1Anwar Alam2Sheeba Zarin3Saurabh Pandey4Hina Singh5Seyed Ehtesham Hasnain6Seyed Ehtesham Hasnain7Nasreen Zafar Ehtesham8Laboratory of Infection Biology and Cell Signaling, Indian Council of Medical Research (ICMR)-National Institute of Pathology, New Delhi, IndiaKusuma School of Biological Sciences, Indian Institute of Technology, Delhi (IIT-D), New Delhi, IndiaLaboratory of Infection Biology and Cell Signaling, Indian Council of Medical Research (ICMR)-National Institute of Pathology, New Delhi, IndiaLaboratory of Infection Biology and Cell Signaling, Indian Council of Medical Research (ICMR)-National Institute of Pathology, New Delhi, IndiaDepartment of Biochemistry, Jamia Hamdard, New Delhi, IndiaDepartment of Biochemical Engineering and Biotechnology, Indian Institute of Technology, Delhi (IIT-D), New Delhi, IndiaDepartment of Biochemical Engineering and Biotechnology, Indian Institute of Technology, Delhi (IIT-D), New Delhi, IndiaDepartment of Life Science, School of Basic Sciences and Research, Sharda University, Greater Noida, IndiaLaboratory of Infection Biology and Cell Signaling, Indian Council of Medical Research (ICMR)-National Institute of Pathology, New Delhi, IndiaMycobacterium tuberculosis (Mtb) is the causative agent of human tuberculosis (TB) which primarily infects the macrophages. Nearly a quarter of the world’s population is infected latently by Mtb. Only around 5%–10% of those infected develop active TB disease, particularly during suppressed host immune conditions or comorbidity such as HIV, hinting toward the heterogeneity of Mtb infection. The aerosolized Mtb first reaches the lungs, and the resident alveolar macrophages (AMs) are among the first cells to encounter the Mtb infection. Evidence suggests that early clearance of Mtb infection is associated with robust innate immune responses in resident macrophages. In addition to lung-resident macrophage subsets, the recruited monocytes and monocyte-derived macrophages (MDMs) have been suggested to have a protective role during Mtb infection. Mtb, by virtue of its unique cell surface lipids and secreted protein effectors, can evade killing by the innate immune cells and preferentially establish a niche within the AMs. Continuous efforts to delineate the determinants of host defense mechanisms have brought to the center stage the crucial role of macrophage phenotypical variations for functional adaptations in TB. The morphological and functional heterogeneity and plasticity of the macrophages aid in confining the dissemination of Mtb. However, during a suppressed or hyperactivated immune state, the Mtb virulence factors can affect macrophage homeostasis which may skew to favor pathogen growth, causing active TB. This mini-review is aimed at summarizing the interplay of Mtb pathomechanisms in the macrophages and the implications of macrophage heterogeneity and plasticity during Mtb infection.https://www.frontiersin.org/articles/10.3389/fimmu.2022.747799/fullMycobacterium tuberculosisinnate immunitymacrophage heterogeneityphenotype switchingmetabolic reprogrammingtrained immunity |
spellingShingle | Faraz Ahmad Anshu Rani Anwar Alam Sheeba Zarin Saurabh Pandey Hina Singh Seyed Ehtesham Hasnain Seyed Ehtesham Hasnain Nasreen Zafar Ehtesham Macrophage: A Cell With Many Faces and Functions in Tuberculosis Frontiers in Immunology Mycobacterium tuberculosis innate immunity macrophage heterogeneity phenotype switching metabolic reprogramming trained immunity |
title | Macrophage: A Cell With Many Faces and Functions in Tuberculosis |
title_full | Macrophage: A Cell With Many Faces and Functions in Tuberculosis |
title_fullStr | Macrophage: A Cell With Many Faces and Functions in Tuberculosis |
title_full_unstemmed | Macrophage: A Cell With Many Faces and Functions in Tuberculosis |
title_short | Macrophage: A Cell With Many Faces and Functions in Tuberculosis |
title_sort | macrophage a cell with many faces and functions in tuberculosis |
topic | Mycobacterium tuberculosis innate immunity macrophage heterogeneity phenotype switching metabolic reprogramming trained immunity |
url | https://www.frontiersin.org/articles/10.3389/fimmu.2022.747799/full |
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