Multifaceted impact of host C-C chemokine CCL2 in the immuno-pathogenesis of HIV-1/M. tuberculosis co-infection

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Abstract

Active tuberculosis remains the leading cause of death among the HIV-1 seropositive individuals. Although significant success has been achieved in bringing down the number of HIV/AIDS-related mortality and morbidity following implementation of highly active anti-retroviral therapy (HAART). Yet, co-infection of Mycobacterium tuberculosis (Mtb) has posed severe clinical and preventive challenges in our efforts to eradicate the virus from the body. Both HIV-1 and Mtb commonly infect macrophages and trigger production of host inflammatory mediators that subsequently regulate the immune response and disease pathogenesis. These inflammatory mediators can impose beneficial or detrimental effects on each pathogen and eventually on host. Among these, inflammatory C-C chemokines play a central role in HIV-1 and Mtb pathogenesis. However, their role in lung-specific mechanisms of HIV-1 and Mtb interaction are poorly understood. In this review we highlight current view on the role of C-C chemokines, more precisely CCL2, on HIV-1: Mtb interaction, potential mechanisms of action and adverse clinical consequences in a setting HIV-1/Mtb co-infection. Targeting common chemokine regulators of HIV-1/Mtb pathogenesis can be an attractive and potential anti-inflammatory intervention in HIV/AIDS-related comorbidities. © 2013 Ansari, Kamarulzaman and Schmidt.

Figures

  • FIGURE 1 | Proposed mechanisms of reciprocal effects of CCL2-mediated immuno-pathogenesis of HIV/Mtb co-infection. HIV-1 infection of alveolar macrophage releases CCL2 that recruits monocytes/macrophages and CD4+T cells at the site of infection hence increase the pool of HIV-1 permissive cells for new round of replication-the feed-back loop model (4, 17) eventually persistence of a high viremia in the BAL. CCL2 can acts on resting CD4+T cells to induce expression of HIV-1 co-receptor CXCR4, thereby rendering them susceptible to infection by X4 strains (38). CCL2 known to trigger differentiation of Th0 toward Th2 phenotype (39) via CCL2–CCR2 axis. Therefore, in the lung a high CCL2 creates a Th2 dominant environment that presumably suppresses Mtb-specific Th1 response. Persistence HIV-1 replication and high viremia in the lung impairs the macrophage and CD4+T cell effector function against Mtb. Most importantly, the targeted apoptosis of CD4+T cells leads to granuloma disruption leading to reactivation and dissemination of latent TB

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Wahid Ansari, A., Kamarulzaman, A., & Schmidt, R. E. (2013). Multifaceted impact of host C-C chemokine CCL2 in the immuno-pathogenesis of HIV-1/M. tuberculosis co-infection. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2013.00312

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