title: Effects of lipopolysaccharide on the expression of proinflammatory cytokines and chemokines and the subsequent recruitment of immunocompetent cells in the oviduct of laying and molting hens.
abstract: The goal of this study was to examine whether lipopolysaccharide (LPS) induces the expression of proinflammatory cytokines and chemokines and recruits T cells in the lower part of the oviduct, and whether that response to LPS is different between the laying and molting phase. White Leghorn laying and molting hens were intravenously injected with saline (control) or LPS. The uterus and vagina of oviducts were collected 3 or 6 h after injection, and used for reverse transcription PCR analysis of IL-1β, IL-6, IL-8 (CXCLi2), and lymphotactin (Lptn), and for immunohistochemical analysis for the frequency of CD4+ and CD8+ T cells. The expressions of IL-1β, IL-6, and CXCLi2 in the uterus and that of IL-1β in the vagina were upregulated in response to LPS 3 or 6 h after injection in both laying and molting hens. The CXCLi2 expression in the vagina was upregulated by LPS in laying hens, whereas those effects of LPS were not significant in molting hens. Expression of Lptn showed a tendency to be downregulated after 3 h, with recovery by 6 h after LPS injection. The frequency of CD4+ T cells tended to increase in response to LPS after 6 h in the lamina propria of the uterus and vagina in both laying and molting hens. The CD8+ T cell frequencies in the lamina propria of the uterus and vagina of laying hens increased in response to LPS after 6 h. However, in the molting hens, LPS stimulation resulted in CD8+ T cell increase in the vagina only and not in the uterus. These results suggest that expressions of proinflammatory cytokines and CXCLi2 chemokine are upregulated in association with T cell recruitment in response to LPS in the lower part of the oviduct, although CD8+ T cells in the uterus may be depressed during the molting phase. These immunoresponses may play roles in the defense against infection of the oviduct.
authors.affiliation: Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nii
authors.forename: Y
authors.initials: Y
authors.lastname: Sonoda
authors.forename: N
authors.initials: N
authors.lastname: Isobe
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshimura
mesh_terms: D000818:Animals; D018791:CD4 Lymphocyte Count; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D018925:Chemokines / Q000235:genetics*; D002645:Chickens / Q000276:immunology* / Q000502:physiology; D016207:Cytokines / Q000235:genetics*; D005260:Female; D007121:Immunocompetence / Q000187:drug effects; D007378:Interleukins / Q000235:genetics; D008070:Lipopolysaccharides / Q000494:pharmacology*; D018655:Lymphocyte Count; D008222:Lymphokines / Q000235:genetics; D018978:Molting / Q000276:immunology; D010057:Oviducts / Q000276:immunology* / Q000378:metabolism*; D010058:Oviposition / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012795:Sialoglycoproteins / Q000235:genetics; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D018925:Chemokines; D016207:Cytokines; D007378:Interleukins; D008070:Lipopolysaccharides; D008222:Lymphokines; D012795:Sialoglycoproteins; C018997:lymphotactin