HIV-1 DOES NOT ALTER IN-VITRO AND IN-VIVO IL-10 PRODUCTION BY HUMAN MONOCYTES AND MACROPHAGES

Citation
A. Bergamini et al., HIV-1 DOES NOT ALTER IN-VITRO AND IN-VIVO IL-10 PRODUCTION BY HUMAN MONOCYTES AND MACROPHAGES, Clinical and experimental immunology, 112(1), 1998, pp. 105-111
Citations number
48
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
112
Issue
1
Year of publication
1998
Pages
105 - 111
Database
ISI
SICI code
0009-9104(1998)112:1<105:HDNAIA>2.0.ZU;2-2
Abstract
The present study analyses the ability of HIV-1 to modulate IL-IO prod uction in cells of monocyte-macrophage lineage cultured in the presenc e of macrophage colony-stimulating factor (M-CSF). Both monocytes and macrophages spontaneously produced low amount of IL-IO. Lipopolysaccha ride (LPS) induced a strong IL-10 response in fresh monocytes and in M -CSF-treated macrophages. In contrast, macrophages cultured in the abs ence of M-CSF exhibited a marked decrease in their susceptibility to L PS stimulation. M-CSF increased the IL-IO response of macrophages to L PS by enhancing both the expression of membrane-bound CD14, the protei n that serves as LPS receptor, and the sensibility of CD14-expressing cells to LPS stimulation. Neither spontaneous nor LPS-induced expressi on of IL-10 was modulated in monocytes and macrophages by infection wi th eight monocytotropic strains, as demonstrated by ELISA and cytofluo rimetric analysis. In contrast, all the HIV-1 strains primed macrophag es for an increased IL-6 response to LPS stimulation. To determine whe ther IL-IO production was associated with in vivo infection, monocytes from AIDS individuals were analysed for IL-10 production. We found th at neither spontaneous nor LPS-induced IL-10 production were different between healthy controls and HIV-infected patients. Taken together, t hese data strongly suggest that HIV-I infection of monocytes-macrophag es does not playa significant role in the regulation of IL-IO in infec ted patients. This study also emphasizes the role of M-CSF activation in the regulation of the cytokine response in macrophages.