title: T. vaginalis Infection Is Associated with Increased IL-8 and TNFr1 Levels but with the Absence of CD38 and HLADR Activation in the Cervix of ESN.
abstract: BACKGROUND
  Trichomonas vaginalis infection is associated with an increased risk of HIV infection in exposed-seronegative women (ESN) despite their unique immune quiescent profile. It is important to understand possible mechanisms, such as recruitment of activated T cells, by which T. vaginalis could facilitate HIV infection in this population.
  
  
  METHODS
  We conducted a cross-sectional study exploring the relationships between T. vaginalis infection, inflammatory markers and T cell activation in the cervix of ESN. During scheduled study visits, participants completed a behavioral questionnaire and physical exam, including sexually transmitted infection (STI) screening and collection of endocervical sponge and cytobrush specimens. T cell and monocyte phenotypes were measured in cervical cytobrush specimens using multi-parameter flow cytometry. Cervical sponge specimens were used to measure cytokines (IL-6, IL-8,IL-10, IP-10, RANTES) using Luminex immunoassays and the immune activation marker soluble TNF receptor 1 using ELISA.
  
  
  RESULTS
  Specimens of 65 women were tested. Twenty-one of these women were infected with T. vaginalis. T. vaginalis infection was associated with significantly increased concentrations of IL-8 (1275pg/ml vs. 566pg/ml, p=.02) and sTNFr1 (430 pg/ml vs. 264 pg/ml, p=.005). However, T. vaginalis infection was not associated with increased percent expression of CCR5+ T cells nor increased CD38 and HLADR activation compared to uninfected women. It was also not associated with increased expression of CCR5+ monocytes.
  
  
  CONCLUSIONS
  Among ESN T. vaginalis infection is associated with increased levels of genital pro-inflammatory/immune activation markers IL-8 and TNFr1, but was not associated with an increased percentage of activated endocervical T cells along the CD38 and HLADR pathways. Thus, while T.vaginalis infection may result in some reversal of the immune quiescent profile of ESN, enhanced recruitment of activated CD38 and HLADR expressing CD4+ cells into the endocervix may not be part of the mechanism by which Trichomonas infection alters HIV susceptibility in this unique subset of women.
authors.affiliation: Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago School of Medicine, Chicago, Illinois, 60612, United States of America.
authors.forename: Olamide D
authors.initials: OD
authors.lastname: Jarrett
authors.affiliation: Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois, 60612, United States of America.
authors.forename: Kirsten E
authors.initials: KE
authors.lastname: Brady
authors.affiliation: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, 21205, United States of America.
authors.forename: Sharada P
authors.initials: SP
authors.lastname: Modur
authors.affiliation: Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois, 60612, United States of America.
authors.forename: Jill
authors.initials: J
authors.lastname: Plants
authors.affiliation: Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois, 60612, United States of America.
authors.forename: Alan L
authors.initials: AL
authors.lastname: Landay
authors.affiliation: Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago School of Medicine, Chicago, Illinois, 60612, United States of America.
authors.forename: Mahmood
authors.initials: M
authors.lastname: Ghassemi
authors.affiliation: Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, 21205, United States of America.
authors.forename: Elizabeth T
authors.initials: ET
authors.lastname: Golub
authors.affiliation: Department of Immunology/Microbiology, Rush University Medical Center, Chicago, Illinois, 60612, United States of America.
authors.forename: Greg T
authors.initials: GT
authors.lastname: Spear
authors.affiliation: Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago School of Medicine, Chicago, Illinois, 60612, United States of America.
authors.forename: Richard M
authors.initials: RM
authors.lastname: Novak
mesh_terms: D000293:Adolescent; D000328:Adult; D002584:Cervix Uteri / Q000382:microbiology*; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000150:complications; D018023:HIV Seronegativity; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism*; D008875:Middle Aged; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000737:chemistry / Q000378:metabolism*; D012995:Solubility; D013601:T-Lymphocytes / Q000166:cytology; D014247:Trichomonas Vaginitis / Q000150:complications / Q000276:immunology / Q000378:metabolism* / Q000821:virology; D014246:Trichomonas vaginalis / Q000502:physiology*; D014779:Virus Replication; D055815:Young Adult
chemical_list: D016209:Interleukin-8; D047888:Receptors, Tumor Necrosis Factor, Type I