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

Olamide D. Jarrett, Kirsten E. Brady, Sharada P Modur, Jill Plants, Alan L. Landay, Mahmood Ghassemi, Elizabeth Golub, Greg T. Spear, Richard M. Novak

Research output: Contribution to journalArticle

Abstract

Introduction: Trichomonas vaginalis infection is associated with an increased risk of HIV infection in exposedseronegative 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.

Original languageEnglish (US)
Article numbere0130146
JournalPLoS One
Volume10
Issue number6
DOIs
StatePublished - Jun 17 2015

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Trichomonas vaginalis
T-cells
cervix
Trichomonas Infections
interleukin-8
Interleukin-8
Cervix Uteri
Chemical activation
Infection
T-lymphocytes
infection
T-Lymphocytes
HIV infections
Porifera
Chemokine CCL5
monocytes
Flow cytometry
Tumor Necrosis Factor Receptors
HIV Infections
Monocytes

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

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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. / Jarrett, Olamide D.; Brady, Kirsten E.; Modur, Sharada P; Plants, Jill; Landay, Alan L.; Ghassemi, Mahmood; Golub, Elizabeth; Spear, Greg T.; Novak, Richard M.

In: PLoS One, Vol. 10, No. 6, e0130146, 17.06.2015.

Research output: Contribution to journalArticle

Jarrett, Olamide D. ; Brady, Kirsten E. ; Modur, Sharada P ; Plants, Jill ; Landay, Alan L. ; Ghassemi, Mahmood ; Golub, Elizabeth ; Spear, Greg T. ; Novak, Richard M. / 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. In: PLoS One. 2015 ; Vol. 10, No. 6.
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abstract = "Introduction: Trichomonas vaginalis infection is associated with an increased risk of HIV infection in exposedseronegative 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.",
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AU - Jarrett, Olamide D.

AU - Brady, Kirsten E.

AU - Modur, Sharada P

AU - Plants, Jill

AU - Landay, Alan L.

AU - Ghassemi, Mahmood

AU - Golub, Elizabeth

AU - Spear, Greg T.

AU - Novak, Richard M.

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N2 - Introduction: Trichomonas vaginalis infection is associated with an increased risk of HIV infection in exposedseronegative 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.

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