Macrophage response to mycobacterium tuberculosis during HIV infection: Relationships between macrophage activation and apoptosis

F. Mariani, D. Goletti, A. Ciaramella, A. Martino, V. Colizzi, M. Fraziano

Research output: Contribution to journalArticlepeer-review

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 monqcytes 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 viceversa, 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.

Original languageEnglish
Pages (from-to)209-216
Number of pages8
JournalCurrent Molecular Medicine
Volume1
Issue number2
Publication statusPublished - 2001

ASJC Scopus subject areas

  • Biochemistry

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