Abstract
Human macrophages represent the first line of defense for the containment of Mycobacterium tuberculosis infection. After phagocytosis, macrophages express activation surface markers and produce proinflammatory cytokines and chemokines whose main role is to control pathogen spreading by recruiting peripheral lymphocytes and monocytes at the site of inflammation. However, in the case of a concomitant human immunodeficiency virus (HIV) infection, these signals strongly enhance the susceptibility to viral infection both at the viral entry and replication levels. Under these conditions, viral expansion extends beyond tissue macrophages to T cells and vice-versa, according to the emerging viral phenotype. In absence of an efficient immune response, Mycobacterium tuberculosis can replicate in macrophages in an uncontrolled fashion culminating in macrophage death by apoptosis. As a consequence, a more severe form of immunedepression, involving both innate and specific immune responses, could be responsible for both ematogenous mycobacterial dissemination and extrapulmonary form of tuberculosis in HIV-infected patients.
Keywords: Macrophage Response, Mycobacterium tuberculosis, Apoptosis, proinflammatory cytokines, chemokines, HIV REPLICATION, BACILLI REPLICATION, T LYMPHOCYTE DEP-LETION, MACROPHAGE APOPTOSIS, Acquired immunodeficiency syndrome
Current Molecular Medicine
Title: Macrophage Response to Mycobacterium tuberculosis During HIV Infection Relationships Between Macrophage Activation and Apoptosis.
Volume: 1 Issue: 2
Author(s): F Mariani, D. Goletti, A. Ciaramella, A. Martino, V. Colizzi and M. Fraziano
Affiliation:
Keywords: Macrophage Response, Mycobacterium tuberculosis, Apoptosis, proinflammatory cytokines, chemokines, HIV REPLICATION, BACILLI REPLICATION, T LYMPHOCYTE DEP-LETION, MACROPHAGE APOPTOSIS, Acquired immunodeficiency syndrome
Abstract: Human macrophages represent the first line of defense for the containment of Mycobacterium tuberculosis infection. After phagocytosis, macrophages express activation surface markers and produce proinflammatory cytokines and chemokines whose main role is to control pathogen spreading by recruiting peripheral lymphocytes and monocytes at the site of inflammation. However, in the case of a concomitant human immunodeficiency virus (HIV) infection, these signals strongly enhance the susceptibility to viral infection both at the viral entry and replication levels. Under these conditions, viral expansion extends beyond tissue macrophages to T cells and vice-versa, according to the emerging viral phenotype. In absence of an efficient immune response, Mycobacterium tuberculosis can replicate in macrophages in an uncontrolled fashion culminating in macrophage death by apoptosis. As a consequence, a more severe form of immunedepression, involving both innate and specific immune responses, could be responsible for both ematogenous mycobacterial dissemination and extrapulmonary form of tuberculosis in HIV-infected patients.
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Mariani F, Goletti D., Ciaramella A., Martino A., Colizzi V. and Fraziano M., Macrophage Response to Mycobacterium tuberculosis During HIV Infection Relationships Between Macrophage Activation and Apoptosis., Current Molecular Medicine 2001; 1 (2) . https://dx.doi.org/10.2174/1566524013363933
DOI https://dx.doi.org/10.2174/1566524013363933 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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