title: Protective antibody therapy is associated with reduced chemokine transcripts in herpes simplex virus type 1 corneal infection.
abstract: Herpes simplex virus type 1 (HSV-1) infection on the murine cornea induces an intense inflammatory response which can lead to blindness. This disease, known as herpes stromal keratitis, can be prevented by the timely passive transfer of monoclonal antibody specific for viral glycoprotein D (gD). Precisely how antibody treatment prevents excessive corneal inflammation is not known. In this study we investigated whether chemokine mRNA expression is inhibited by antibody treatment. Total cellular RNAs isolated from normal corneas and at various times after virus infection were analyzed via reverse transcription-PCR for mRNA coding for seven different chemokines. Constitutive levels of IP-10, KC, MIP-2, MCP-1, MIP-1 beta, and RANTES mRNA were detected in uninfected corneas of BALB/c mice. When the cornea was mechanically traumatized, message for all six chemokines was transiently elevated above constitutive levels. In contrast, HSV-1 infection resulted in prolonged enhanced chemokine message expression. The kinetics of mRNA accumulation was distinctive for each chemokine analyzed. MIP-1 alpha message, not detected constitutively, was not evident until day 7 postinfection. Administration of anti-HSV gD monoclonal antibody 1 day after infection was associated with reduced message for MIP-2, MCP-1, MIP-1 alpha, and MIP-1 beta. IP-10, KC, and RANTES messages were not altered. Collectively, our results suggest that anti-gD treatment may protect, at least in part, by inhibiting production of chemokines believed to promote inflammation.
authors.affiliation: Department of Microbiology and Immunology, University of South Alabama, Mobile 36688, USA.
authors.forename: Y H
authors.initials: YH
authors.lastname: Su
authors.forename: X T
authors.initials: XT
authors.lastname: Yan
authors.forename: J E
authors.initials: JE
authors.lastname: Oakes
authors.forename: R N
authors.initials: RN
authors.lastname: Lausch
mesh_terms: D000818:Animals; D000914:Antibodies, Viral / Q000008:administration & dosage* / Q000276:immunology; D001483:Base Sequence; D054357:Chemokine CXCL10; D018925:Chemokines / Q000096:biosynthesis* / Q000235:genetics; D019743:Chemokines, CXC; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D017931:DNA Primers; D004195:Disease Models, Animal; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000276:immunology*; D006801:Humans; D007116:Immunization, Passive; D016849:Keratitis, Herpetic / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000096:biosynthesis; D014759:Viral Envelope Proteins / Q000276:immunology
chemical_list: D000914:Antibodies, Viral; D054357:Chemokine CXCL10; D018925:Chemokines; D019743:Chemokines, CXC; D016207:Cytokines; D017931:DNA Primers; D012333:RNA, Messenger; D014759:Viral Envelope Proteins; C039447:glycoprotein D, Human herpesvirus 1