title: Differential Expression of mRNA Encoding Cytokines and Chemokines in the Reproductive Tract after Infection of Mice withChlamydia trachomatis.
abstract: Infection withChlamydia trachomatistargets epithelial cells within the genital tract which respond by secreting chemokines and cytokines. Persistent inflammation can lead to fibrosis, tubal infertility and/or ectopic pregnancy; many infections are asymptomatic. Most studies have investigated the inflammatory response in the initial stages of infection, less is known about the later stages of infection, especially with a low, potentially asymptomatic, bacterial load. Our objective was to determine the inflammatory mediators involved in clearance of low-grade infection and the potential involvement in chronic inflammation. Six to eight week old C3H/HeJ mice were pretreated with 2.5 mg medroxyprogesterone acetate on day -10 and -3 before infection. Mice (n=3 for 28 d, n=3 for 35 d) were infected with 5 × 102inclusion-forming units ofC. trachomatis, serovar D; vaginal cultures were obtained weekly to monitor infection. Control mice (n=3 for 28 d, n=3 for 35 d) were sham infected. Mice were killed on day 28 (experiment 1) and day 35 (experiment 2) post-infection and vaginal tissue, uterine horns and oviducts collected for analysis of mRNAs encoding inflammatory cytokines and chemokines. Total RNA was isolated and a superarray analysis performed using mouse Cytokines and Chemokines PCR arrays (Qiagen, Valencia, CA). Statistical differences in gene expression were determined using a paired Students t-test. At 28 days after infection, the expression of mRNA encoding 6, 35 and 3 inflammatory genes differed from controls in vaginal, uterine and oviductal tissues, respectively (P<0.05). At 35 days after infection, the expression of mRNA encoding 16, 38 and 14 inflammatory genes differed from controls in vaginal, uterine and oviductal tissues, respectively (P<0.05). Understanding the mechanisms involved in the inflammatory response at later stages of infection should aid in the development of treatment options that minimize the development of asymptomatic, chronic inflammation-induced infertility.
authors.affiliation: Department of Animal and Food Sciences, University of Kentucky, Lexington, KY, USA.
authors.forename: Katheryn L
authors.initials: KL
authors.lastname: Cerny
authors.affiliation: Department of Animal and Food Sciences, University of Kentucky, Lexington, KY, USA.
authors.forename: Maranda
authors.initials: M
authors.lastname: Van Fleet
authors.affiliation: Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA, USA.
authors.forename: Anatoly
authors.initials: A
authors.lastname: Slepenkin
authors.affiliation: Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA, USA.
authors.forename: Ellena M
authors.initials: EM
authors.lastname: Peterson
authors.affiliation: Department of Animal and Food Sciences, University of Kentucky, Lexington, KY, USA.
authors.forename: Phillip J
authors.initials: PJ
authors.lastname: Bridges
keywords: Chemokines; Chlamydia trachomatis; Cytokines; Immune response; Inflammation; Oviduct