Responsiveness of human polymorphonuclear cells (PMNL) to stimulation by a mannoprotein fraction (MP-F2) of Candida albicans; enhanced production of IL-6 and tumour necrosis factor-alpha (TNF-alpha) by MP-F2-stimulated PMNL from HIV-infected subjects.
IL-1beta, IL-6, IL-8 and TNF-alpha production by PMNL from 21 HIV-infected (HIV+), including 11 full-blown AIDS, and 20 HIV-uninfected (HIV-) subjects (matched for age and sex to HIV+ ones) was studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and ELISA. PMNL from both categories of subjects were strongly stimulated in their actual cytokine production by a mannoprotein fraction (MP-F2) of Candida albicans, as well as by the bacterial lipopolysaccharide (LPS). These stimulatory effects were apparently due to increased cytokine gene expression and were substantially reversed by the physiological inhibitor IL-10. However, PMNL from HIV+ subjects showed increased IL-6 and TNF-alpha gene expression and produced more IL-6 and TNF-alpha than PMNL from HIV- controls, under similar stimulation conditions. This difference could not be attributed to a given stage of HIV infection, any associated medication, or to a generalized increase of gene expression, as quantitatively similar beta-actin and IL-1beta transcripts were detected. Moreover, no significant difference in IL-8 production by the PMNL from HIV+ and HIV- subjects was observed. Our studies suggest that PMNL from HIV+ subjects might add to other cellular sources of IL-6 and TNF-alpha (e.g. monocytes-macrophages) in contributing to the cytokine-dysregulated pattern typical of the HIV+ patient.
Torosantucci
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Department of Bacteriology and Medical Mycology, Istituto Superiore di Sanità, University of Rome La Sapienza, Italy.
Chiani
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Quinti
I
I
Ausiello
C M
CM
Mezzaroma
I
I
Cassone
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A
D000328:Adult; D002176:Candida albicans / Q000276:immunology; D002478:Cells, Cultured; D005260:Female; D005656:Fungal Proteins / Q000276:immunology* / Q000494:pharmacology; D015658:HIV Infections / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000494:pharmacology; D015850:Interleukin-6 / Q000096:biosynthesis*; D016209:Interleukin-8 / Q000096:biosynthesis; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology* / Q000494:pharmacology; D008875:Middle Aged; D018375:Neutrophil Activation / Q000187:drug effects / Q000276:immunology*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology*; D010446:Peptide Fragments / Q000276:immunology* / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D005656:Fungal Proteins; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008562:Membrane Glycoproteins; D010446:Peptide Fragments; D014409:Tumor Necrosis Factor-alpha; C025363:mannoproteins; D016753:Interleukin-10