Repeated social stress enhances the innate immune response to a primary HSV-1 infection in the cornea and trigeminal ganglia of Balb/c mice.
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.
Dong-Newsom
P
P
The Ohio State University, College of Dentistry, Section of Oral Biology, Genetics, Columbus, OH 43210, USA.
Powell
N D
ND
Bailey
M T
MT
Padgett
D A
DA
Sheridan
J F
JF
D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D003315:Cornea / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D016207:Cytokines / Q000096:biosynthesis; D005434:Flow Cytometry; D015870:Gene Expression / Q000502:physiology; D006561:Herpes Simplex / Q000276:immunology* / Q000523:psychology* / Q000821:virology; D018259:Herpesvirus 1, Human; D007113:Immunity, Innate / Q000502:physiology*; D008264:Macrophages / Q000378:metabolism / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012931:Social Environment; D013315:Stress, Psychological / Q000276:immunology*; D012668:Trigeminal Ganglion / Q000276:immunology* / Q000378:metabolism / Q000821:virology*; D014764:Viral Proteins / Q000096:biosynthesis / Q000235:genetics
D039481:CD11b Antigen; D016207:Cytokines; D014764:Viral Proteins; D012313:RNA