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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 OD, Brady KE, Modur SP, Plants J, Landay AL, Ghassemi M, Golub ET, Spear GT, Novak RM - PLoS ONE (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago School of Medicine, Chicago, Illinois, 60612, United States of America.

ABSTRACT

Introduction: 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.

No MeSH data available.


Related in: MedlinePlus

Cytokines and sTNFr1 endocervical expression.Data represents median and interquartile range. TV = Trichomonas vaginalis. P values are the result of Mann-Whitney test.
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pone.0130146.g001: Cytokines and sTNFr1 endocervical expression.Data represents median and interquartile range. TV = Trichomonas vaginalis. P values are the result of Mann-Whitney test.

Mentions: Fig 1 shows the relationship between endocervical cytokines/inflammatory markers and T. vaginalis infection. With the exception of IL-8, cytokine concentrations were low in this ESN population, with the following percentage of values falling below the LLD: of IL-6 20%, IL-10 72%, IP-10 17%, and RANTES 26%. T.vaginalis infection was associated with increase expression of IL-8 compared to uninfected women (1275pg/ml vs. 566 pg/ml, p = .02) and a trend toward increased expression of IL-6 (p = .07). T. vaginalis was also significantly associated with increased expression of the immune activation marker, sTNFr1 (430 pg/ml versus 264 pg/ml, p = 0.0005). There was no significant effect of T. vaginalis infection on the endocervical levels of IL-10, IP-10, or RANTES.


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 OD, Brady KE, Modur SP, Plants J, Landay AL, Ghassemi M, Golub ET, Spear GT, Novak RM - PLoS ONE (2015)

Cytokines and sTNFr1 endocervical expression.Data represents median and interquartile range. TV = Trichomonas vaginalis. P values are the result of Mann-Whitney test.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4470998&req=5

pone.0130146.g001: Cytokines and sTNFr1 endocervical expression.Data represents median and interquartile range. TV = Trichomonas vaginalis. P values are the result of Mann-Whitney test.
Mentions: Fig 1 shows the relationship between endocervical cytokines/inflammatory markers and T. vaginalis infection. With the exception of IL-8, cytokine concentrations were low in this ESN population, with the following percentage of values falling below the LLD: of IL-6 20%, IL-10 72%, IP-10 17%, and RANTES 26%. T.vaginalis infection was associated with increase expression of IL-8 compared to uninfected women (1275pg/ml vs. 566 pg/ml, p = .02) and a trend toward increased expression of IL-6 (p = .07). T. vaginalis was also significantly associated with increased expression of the immune activation marker, sTNFr1 (430 pg/ml versus 264 pg/ml, p = 0.0005). There was no significant effect of T. vaginalis infection on the endocervical levels of IL-10, IP-10, or RANTES.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago School of Medicine, Chicago, Illinois, 60612, United States of America.

ABSTRACT

Introduction: 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.

No MeSH data available.


Related in: MedlinePlus