Human beta defensin-3 (hBD-3) is an antimicrobial peptide with diverse functionality. We investigated the capacity of hBD-3 and for comparison, Pam3CSK4 and LL-37, to induce co-stimulatory molecules and chemokine expression in monocytes. These stimuli differentially induced CD80 and CD86 on the surface of monocytes and each stimulant induced a variety of chemokines including MCP-1, Gro-alpha, MDC and Mip1beta, while only hBD-3 and Pam3CSK4 significantly induced the angiogenesis factor, Vascular endothelial growth factor. HBD-3 induced similar chemokines in monocyte-derived macrophages and additionally induced expression of RANTES in these cells. Comparison of monocytes from HIV+ and HIV- donors indicated that monocytes from HIV+ donors were more likely to spontaneously express certain chemokines (Mip1alpha, Mip1beta and MCP-1) and less able to increase expression of other molecules in response to hBD-3 (MDC, Gro-alpha and VEGF). Chemokine receptor expression (CCR5, CCR2 and CXCR2) was relatively normal in monocytes from HIV+ donors compared to cells from HIV- donors with the exception of diminished expression of the receptor for MDC, CCR4, which was reduced in the patrolling monocyte subset (CD14+CD16++) of HIV+ donors. These observations implicate chemokine induction by hBD-3 as a potentially important mechanism for orchestrating cell migration into inflamed tissues. Alterations in chemokine production or their receptors in monocytes of HIV-infected persons could influence cell migration and modify the effects of hBD-3 at sites of inflammation. This article is protected by copyright. All rights reserved.
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