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Impaired phagocyte oxidative capacity in human immunodeficiency virus-infected children
K C Hayani1, S C Verral, D L Pitrak
1Division of Pediatric Infectious Diseases, Department of Pediatrics, University of Illinois College of Medicine at Chicago, Chicago, IL 60612-7324, USA. U12017@UIC.edu
Insights
Human immunodeficiency virus (HIV) impairs phagocyte function in children, increasing bacterial infection risk. Respiratory burst capacity is reduced, particularly in those with severe CD4 T-cell depletion.
Area of Science:
- Immunology
- Pediatrics
- Infectious Diseases
Background:
- Children with human immunodeficiency virus (HIV) exhibit T helper cell deficiency.
- Frequent bacterial infections in HIV-infected children suggest underlying phagocyte dysfunction.
Purpose of the Study:
- To investigate the respiratory burst capacity of phagocytes in HIV-infected children.
- To compare phagocyte function between HIV-infected, HIV-exposed uninfected, and healthy children.
Main Methods:
- Whole blood chemiluminescence (CL) assays were employed to measure phagocyte respiratory burst capacity.
- Phagocytes were stimulated using zymosan opsonized with human complement, with and without priming agents like platelet-activating factor (PAF) or FMLP.
- Enzyme activities (oxidase, myeloperoxidase) were assessed following stimulation with phorbol myristate acetate (PMA).
Main Results:
- Unprimed CL responses to opsonized zymosan were significantly decreased in HIV-infected children with severe CD4 T-cell suppression (P=.03).
- PAF-primed CL responses were reduced in HIV-infected children with moderate (P=.02) and severe (P=.01) CD4 T-cell suppression.
- These functional impairments occurred despite normal or elevated activities of key respiratory burst enzymes.
Conclusions:
- Phagocyte respiratory burst capacity is impaired in HIV-infected children, correlating with CD4 T-cell counts.
- This phagocyte dysfunction may contribute to the increased susceptibility to secondary bacterial infections in this population.
Abstract:
Children infected with the human immunodeficiency virus (HIV) have T helper cell deficiency, but frequent bacterial infections suggest phagocyte dysfunction. Whole blood chemiluminescence (CL) assays were used to measure the respiratory burst capacity of phagocytes from HIV-infected children, perinatally HIV-exposed but uninfected children, and normal healthy children. Phagocytes were stimulated by zymosan opsonized with human complement with and without priming by platelet-activating factor (PAF) or FMLP. Activities of enzymes involved in the respiratory burst, oxidase and myeloperoxidase, were examined after opsonin receptor-independent stimulation with PMA. Unprimed CL responses to opsonized zymosan were decreased for HIV-infected children with severe CD4 lymphocyte suppression compared with healthy children (P=.03), and PAF-primed CL responses to opsonized zymosan were decreased in HIV-infected children with both moderate and severe CD4 lymphocyte suppression (P=.02 and P=.01, respectively), despite normal or increased activities of the respiratory burst enzymes. These impairments may contribute to secondary bacterial infections.