PMID- 19822203 OWN - NLM STAT- MEDLINE DCOM- 20100423 LR - 20211020 IS - 1090-2139 (Electronic) IS - 0889-1591 (Print) IS - 0889-1591 (Linking) VI - 24 IP - 2 DP - 2010 Feb TI - Repeated social stress enhances the innate immune response to a primary HSV-1 infection in the cornea and trigeminal ganglia of Balb/c mice. PG - 273-80 LID - 10.1016/j.bbi.2009.10.003 [doi] AB - Three to 5 days after a primary HSV-1 infection, macrophages infiltrate into the trigeminal ganglia (TG) and produce anti-viral cytokines to reduce viral replication. Previous research demonstrated that social disruption stress (SDR) enhances the trafficking of monocytes/macrophages from the bone marrow to the spleen and increases pro-inflammatory cytokine production in vitro and in vivo. The impact of SDR on the trafficking of these cells to loci of herpes simplex virus type 1 (HSV-1) infection and subsequent function has not been examined. The following studies were designed to determine whether SDR would enhance the innate immune response during a primary HSV-1 infection by increasing the number of macrophages in the cornea and TG, thus increasing anti-viral cytokine production and reducing viral replication. BALB/c mice were exposed to six cycles of SDR prior to ocular infection with HSV-1 McKrae virus. Flow cytometric analysis of cells from the TG revealed an increase in the percentage of CD11b+ macrophages in SDR mice compared to controls. Immune cell infiltration into the cornea, however, could not be determined due to low cell numbers. Although gene expression of IFN-beta was decreased, SDR increased gene expression of IFN-alpha, and TNF-alpha, in the cornea and TG. Examination of viral proteins showed decreased expression of infected cell protein 0 (ICP0), glycoprotein B (gB), glycoprotein H (gH) and latency-associated transcript (LAT) in the TG, however, expression of ICP0 and gB were elevated in the cornea of SDR mice. These results indicate that the innate immune response to HSV-1 was altered and enhanced by the experience of repeated social defeat. CI - Copyright 2009 Elsevier Inc. All rights reserved. FAU - Dong-Newsom, P AU - Dong-Newsom P AD - The Ohio State University, College of Dentistry, Section of Oral Biology, Genetics, Columbus, OH 43210, USA. FAU - Powell, N D AU - Powell ND FAU - Bailey, M T AU - Bailey MT FAU - Padgett, D A AU - Padgett DA FAU - Sheridan, J F AU - Sheridan JF LA - eng GR - T32 DE014320-07/DE/NIDCR NIH HHS/United States GR - R01 MH046801/MH/NIMH NIH HHS/United States GR - R01MH046801-18/MH/NIMH NIH HHS/United States GR - T32DE014320-07/DE/NIDCR NIH HHS/United States GR - T32 DE014320/DE/NIDCR NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20091012 PL - Netherlands TA - Brain Behav Immun JT - Brain, behavior, and immunity JID - 8800478 RN - 0 (CD11b Antigen) RN - 0 (Cytokines) RN - 0 (Viral Proteins) RN - 63231-63-0 (RNA) SB - IM MH - Animals MH - CD11b Antigen/metabolism MH - Cornea/*immunology/metabolism/*virology MH - Cytokines/biosynthesis MH - Flow Cytometry MH - Gene Expression/physiology MH - Herpes Simplex/*immunology/*psychology/virology MH - *Herpesvirus 1, Human MH - Immunity, Innate/*physiology MH - Macrophages/metabolism/physiology MH - Male MH - Mice MH - Mice, Inbred BALB C MH - RNA/biosynthesis/isolation & purification MH - Reverse Transcriptase Polymerase Chain Reaction MH - *Social Environment MH - Stress, Psychological/*immunology MH - Trigeminal Ganglion/*immunology/metabolism/*virology MH - Viral Proteins/biosynthesis/genetics PMC - PMC2818401 MID - NIHMS157544 EDAT- 2009/10/14 06:00 MHDA- 2010/04/24 06:00 PMCR- 2011/02/01 CRDT- 2009/10/14 06:00 PHST- 2009/06/15 00:00 [received] PHST- 2009/09/22 00:00 [revised] PHST- 2009/10/05 00:00 [accepted] PHST- 2009/10/14 06:00 [entrez] PHST- 2009/10/14 06:00 [pubmed] PHST- 2010/04/24 06:00 [medline] PHST- 2011/02/01 00:00 [pmc-release] AID - S0889-1591(09)00467-X [pii] AID - 10.1016/j.bbi.2009.10.003 [doi] PST - ppublish SO - Brain Behav Immun. 2010 Feb;24(2):273-80. doi: 10.1016/j.bbi.2009.10.003. Epub 2009 Oct 12.