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In the present paper we assessed the role of Fas in the expression of pro-inflammatory cytokines and chemokines during HSV-2 infection using keratinocyte and monocyte cells in vitro. While uninfected keratinocyte and monocyte cultures responded with apoptosis induction upon Fas receptor stimulation with cytotoxic antibody, HSV-2-infected monocytes, but not keratinocytes, were susceptible to Fas-induced apoptosis. Both uninfected, Fas-stimulated and HSV-2-infected keratinocytes and only infected mono cytes up-regulated the expression of pro-inflammatory chemokines – chemokine (C-X-C motif) ligand 1 (CXCL1) and CXCL10 and cytokines – interferon α (IFN- α) and tumour necrosis factor α (TNF- α). HSV-2 infection of monocytes and keratinocytes led to up-regulation of TNF- α, IFN- α, CXCL1 and CXCL10 expression. Stimulation of Fas receptor reduced the expression of tested cytokines and chemokines in HSV-2-infected keratinocyte cultures, but not in monocytes. Furthermore, while apopto sis blocking down-regulated the expression of IFN- α, CXCL1 and CXCL10 in HSV-2-infected mono cytes, the keratinocytes showed the opposite effect for IFN- α, and CXCL10. We conclude that the Fas/FasL pathway participates in controlling the pro-inflammatory response during HSV-2 infection, albeit its effect depends on the type of infected cells.

Experimental immunology HSV-2-infected monocytes and keratinocytes show different inflammatory reaction in response to Fas receptor stimulation