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-Chemokines in Human Peripheral Blood Monocytes Through a CD4-Independent Mechanism1
Laboratory of Virology, Istituto Superiore di Sanità, Rome, Italy
The present study was designed to evaluate the effect of the HIV-1
envelope glycoprotein gp120 on the expression of 
-chemokines in
cultured monocytes/macrophages. Treatment of either freshly isolated
1-day-cultured monocytes or 7-day-cultured monocyte-derived macrophages
(MDM) with recombinant gp120-IIIB resulted in a specific and
dose-dependent enhancement of secretion of monocyte chemoattractant
protein-1, macrophage inflammatory protein-1, and RANTES as well as
a clear-cut increase in transcript accumulation. The expression of
these mRNA was increased, but not superinduced, in the presence of
cycloheximide. -Chemokine secretion was also induced after exposure
of monocyte cultures to gp120-JRFL and aldrithiol-2-inactivated R5 and
X4 HIV-1 strains, retaining conformational and functional integrity of
envelope proteins. In contrast, no -chemokine secretion was
triggered by X4 and R5 gp120 or aldrithiol-2-inactivated virus
treatment of monocytoid cell lines that were fully responsive to LPS.
The gp120-mediated effect was independent of its interaction with CD4,
as preincubation with soluble CD4 did not abrogate -chemokine
induction. Moreover, triggering of CD4 receptor by a specific Ab did
not result in any -chemokine secretion. Interestingly, engagement of
CCR5 and CXCR4 receptors by specific Abs as well as treatment with CCR5
and CXCR4 ligands induced -chemokine secretion. On the whole, these
results indicate that HIV-1 stimulates monocytes/macrophages to produce
-chemokines by a specific interaction of gp120 with HIV-1
coreceptors on the cell membrane. The expression of these related
polypeptides may represent an important cellular response for
regulating both the extent of viral infection and the recruitment of
immune cells.
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