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Apical interactions of HIV type 1 with polarized HEC-1 cell monolayer modulate R5-HIV type 1 spread by submucosal macrophages. | LitMetric

Apical interactions of HIV type 1 with polarized HEC-1 cell monolayer modulate R5-HIV type 1 spread by submucosal macrophages.

AIDS Res Hum Retroviruses

Université Paris Descartes (Paris V), Unité INSERM U743 Immunologie Humaine, Equipe Immunité et Biothérapie Muqueuse, Centre de Recherches Biomédicales des Cordeliers, Paris, France.

Published: May 2009

AI Article Synopsis

Article Abstract

The in vitro model of HIV-1 transcytosis through a monolayer of HEC-1 cells is thought to mimic the mucosal crossing of the virus that may occur in vivo. We evaluated whether the stimulation of HEC-1 by HIV may modulate HIV infection of macrophages. Thus, the ability to capture, produce, and transfer R5 viruses to T cells, attract T cells, and finally produce cytokines/chemokines, was compared between untreated macrophages (M0) and macrophages differentiated in the presence of medium collected at the basolateral pole of HEC-1, which were unstimulated [M(BL)] or stimulated with either R5-HIV-1Ba-L [M(BL-R5)] or X4-HIV-1NDK [M(BL-X4)]. M(BL-X4)-secreted CCR5-interacting chemokines integrated and replicated HIV less efficiently than did M(BL) and M(BL-R5). M(BL-R5) and M(BL-X4) similarly transmitted HIV to activated T cells. Interestingly, mannose-binding receptors and heparan sulfate proteoglycans were variously involved in HIV adsorption, whereas DC-SIGN mostly mediated the HIV transfer. Conversely to M(BL) and M(BL-X4), M(BL-R5) did not secrete eotaxin, GRO, ITAC, lymphotactin, MIP-1, MIP-3, and RANTES, which was associated with a weak capacity to recruit CD4(+)CXCR4(+)CCR5(+) T cells. In particular, M(BL-R5) specifically released soluble factors enhancing HIV production by recruited T cells. These submucosal-conditioned macrophages differentially captured, produced, and transferred R5-HIV-1 to T cells, according to the tropism of the virus deposited at the apical pole of HEC-1. These observations challenge the question of the in vivo involvement of HIV-1 as a supraepithelial stimulus that likely modulates the susceptibility for HIV-1 of submucosal target cells in favor of its transmission.

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Source
http://dx.doi.org/10.1089/aid.2008.0156DOI Listing

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