Human immunodeficiency virus (HIV) replicates more efficiently in Mycobacterium tuberculosis (MTB)-infected macrophages than in uninfected controls. We investigated whether this may be partly explained by changes in expression of CCR5 in the course of mycobacterial infection, as this molecule has been shown to be a coreceptor for HIV entry. Since the lung is the preferential organ of HIV replication in the course of tuberculosis, we preliminarily analyzed beta-chemokine receptor expression in alveolar macrophages from patients with active tuberculosis, using flow cytometry based on an MIP-1 alpha ligand-biotin/avidin-FITC detection system. Increased MIP-1 alpha receptor (MIP-1 alpha R) expression in alveolar macrophages from infected patients was observed whereas no detectable expression could be revealed in uninfected controls. Since MIP-1 alpha can also bind CCR1 and CCR4, the presence of CCR5 mRNA was investigated in bronchoalveolar lavage (BAL) cells and detected in alveolar macrophages from tuberculosis patients only. The study was then extended to in vitro MTB-infected macrophages, Monocyte-derived macrophages (MDMs) were left to differentiate for 7 days before MTB H37Rv infection, and CCR5 expression was monitored, by using a specific monoclonal antibody, on days 1, 6, and 11 after infection. Increased CCR5 expression in MTB-infected macrophages was observed, with a peak on day 6 (64% in MTB-infected versus 33% in control cultures) and a decrease by day 11 (25% in MTB infected versus 13% in control cultures). These results show that CCR5 expression is enhanced in the course of in vitro MTB infection and during active pulmonary tuberculosis.

Fraziano, M., Cappelli, G., Santucci, M., Mariani, F., Amicosante, M., Casarini, M., et al. (1999). Expression of CCR5 is increased in human monocyte-derived macrophages and alveolar macrophages in the course of in vivo and in vitro Mycobacterium tuberculosis infection. AIDS RESEARCH AND HUMAN RETROVIRUSES, 15(10), 869-874 [10.1089/088922299310575].

Expression of CCR5 is increased in human monocyte-derived macrophages and alveolar macrophages in the course of in vivo and in vitro Mycobacterium tuberculosis infection

FRAZIANO, MAURIZIO;AMICOSANTE, MASSIMO;COLIZZI, VITTORIO
1999-01-01

Abstract

Human immunodeficiency virus (HIV) replicates more efficiently in Mycobacterium tuberculosis (MTB)-infected macrophages than in uninfected controls. We investigated whether this may be partly explained by changes in expression of CCR5 in the course of mycobacterial infection, as this molecule has been shown to be a coreceptor for HIV entry. Since the lung is the preferential organ of HIV replication in the course of tuberculosis, we preliminarily analyzed beta-chemokine receptor expression in alveolar macrophages from patients with active tuberculosis, using flow cytometry based on an MIP-1 alpha ligand-biotin/avidin-FITC detection system. Increased MIP-1 alpha receptor (MIP-1 alpha R) expression in alveolar macrophages from infected patients was observed whereas no detectable expression could be revealed in uninfected controls. Since MIP-1 alpha can also bind CCR1 and CCR4, the presence of CCR5 mRNA was investigated in bronchoalveolar lavage (BAL) cells and detected in alveolar macrophages from tuberculosis patients only. The study was then extended to in vitro MTB-infected macrophages, Monocyte-derived macrophages (MDMs) were left to differentiate for 7 days before MTB H37Rv infection, and CCR5 expression was monitored, by using a specific monoclonal antibody, on days 1, 6, and 11 after infection. Increased CCR5 expression in MTB-infected macrophages was observed, with a peak on day 6 (64% in MTB-infected versus 33% in control cultures) and a decrease by day 11 (25% in MTB infected versus 13% in control cultures). These results show that CCR5 expression is enhanced in the course of in vitro MTB infection and during active pulmonary tuberculosis.
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/04 - Patologia Generale
English
Con Impact Factor ISI
chemokine receptor ccr5; macrophage inflammatory protein 1alpha; monoclonal antibody; antibody specificity; article; base pairing; DNA content; flow cytometry; gene deletion; human; human cell; human immunodeficiency virus 1; lung alveolus macrophage; lung lavage; macrophage activation; mycobacterium tuberculosis; priority journal; tuberculosis; virus replication; Cells, Cultured; Female; HIV-1; Humans; Macrophage Inflammatory Protein-1; Macrophages; Macrophages, Alveolar; Male; Monocytes; Mycobacterium tuberculosis; Receptors, CCR5; Receptors, Chemokine; Tuberculosis, Pulmonary
Fraziano, M., Cappelli, G., Santucci, M., Mariani, F., Amicosante, M., Casarini, M., et al. (1999). Expression of CCR5 is increased in human monocyte-derived macrophages and alveolar macrophages in the course of in vivo and in vitro Mycobacterium tuberculosis infection. AIDS RESEARCH AND HUMAN RETROVIRUSES, 15(10), 869-874 [10.1089/088922299310575].
Fraziano, M; Cappelli, G; Santucci, M; Mariani, F; Amicosante, M; Casarini, M; Giosue, S; Bisetti, A; Colizzi, V
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/43530
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