Brief Report: HIV-1 Infection Impairs CD16 and CD35 Mediated Opsonophagocytosis of Mycobacterium tuberculosis by Human Neutrophils.

J Acquir Immune Defic Syndr

*Clinical Infectious Diseases Research Initiative, Institute for Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa; †Institute of Tropical Medicine, Antwerp, Belgium; ‡Medical Research Council (MRC)/Uganda Virus Research Institute (UVRI) Uganda Research Unit on AIDS, Entebbe, Uganda; §Blizard Institute, Barts and The London School of Medicine, Queen Mary University of London, London, United Kingdom; ‖Department of Medicine, Imperial College London, London, United Kingdom; ¶Mill Hill Laboratory, The Francis Crick Institute, London, United Kingdom; and #Institute of Immunity and Transplantation, University College London, London, United Kingdom.

Published: November 2016

Using a flow cytometric assay, we investigated neutrophil-Mycobacterium tuberculosis opsonophagocytosis and the impact of HIV-1-infected serum on this process. The mean (±SD) percentage of neutrophils internalizing bacilli after 30 minutes incubation was significantly reduced by pretreatment with anti-CD16 (18.2% ± 8.1%, P < 0.001) or anti-CD35 antibody (23.2% ± 10.6%, P < 0.05) versus anti-CD4 controls (29.9% ± 8.1%). Blocking CD88 or CD11a did not affect internalization. Using heat-inactivated serum, maximal internalization was lower using HIV-1-infected serum versus HIV-1-uninfected. Using non-heat-inactivated serum, internalization decreased more rapidly with sequential dilutions of HIV-1-infected versus HIV-1-uninfected serum. CD16 and CD35 are important for neutrophil internalization of M. tuberculosis, whereas HIV-1 infection adversely affects opsonophagocytosis.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5018214PMC
http://dx.doi.org/10.1097/QAI.0000000000001103DOI Listing

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