Premium
Relationship Between Interleukin‐5 Production and Variations in Eosinophil Counts During HIV Infection in West Africa: Influence of Mycobacterium tuberculosis Infection
Author(s) -
DIAGBOUGA S.,
ALDEBERT D.,
FUMOUX F.,
CAPRON M.,
LEDRU E.
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00467.x
Subject(s) - immunology , eosinophil , ionomycin , tuberculosis , peripheral blood mononuclear cell , medicine , mycobacterium tuberculosis , cytokine , eosinopenia , immune system , interleukin 5 , virology , biology , interleukin , pathology , in vitro , stimulation , biochemistry , asthma
Eosinophils are important effectors of the non‐specific immune response and we studied whether perturbations in the production of the type 2 cytokine, interleukin‐5 (IL‐5), could account for the variations in eosinophil counts observed in human immunodeficiency virus (HIV) infection. HIV‐infected patients without helminthiasis were investigated in a cross‐sectional study in West Africa. Eosinophil counts were significantly higher in CDC‐B patients than in controls, but were dramatically decreased at the CDC‐C stage. Phorbol 12‐myristate 13‐acetate (PMA) + ionomycin‐induced IL‐5 production by peripheral blood mononuclear cells (PBMC) was decreased from the A stage of the disease, and significant correlations were observed between IL‐5 production and eosinophil counts in tuberculosis (TB)‐negative HIV‐1‐positive, TB‐positive HIV‐1‐positive and TB‐positive HIV‐negative patient groups. Nevertheless, the production of IL‐5 was not decreased in HIV‐positive patients with TB, in contrast to HIV‐positive patients without TB presenting with the same ranges of CD4 + counts. Our data suggest that, during HIV infection, the impairment in IL‐5 production is one of the factors associated with the ‘paradoxal’ eosinopenia observed in tropical areas, but that IL‐5 production during active TB is compensated by cellular subsets, yet to be identified.