Adolescent health briefMucosal Immunity of the Adolescent Female Genital Tract☆
Section snippets
Methods
Female patients aged 15 to 17 years attending the Adolescent/Young Adult Clinic, Children’s Hospital Boston were eligible if they were at least 2 years past menarche, had regular menstrual cycles, had initiated sexual intercourse but would abstain during the study, and had a normal Papanicolaou smear within the previous 6 months. Exclusion criteria included pregnancy, current tobacco use, autoimmune disease or other immunodeficiency, an abnormal gastrointestinal tract, use of immunosuppressive
Results
Three adolescents (16.8 ± 0.8 years old) were each followed through one menstrual cycle; one participant was followed during an additional cycle owing to missed study visits around the time of ovulation. Participants were 4.2 ± 0.9 years postmenarche and sexually active for 2.5 ± 0.4 years.
IgA concentrations (Table 1) varied throughout the menstrual cycle, with levels lower at ovulation and higher in the follicular and luteal phases. IL-6 and IL-8 concentrations differed similarly across the
Discussion
Our findings indicate that, similar to adults, ovulatory adolescents experience changes in concentrations of IgA, IgG, and cytokines in cervical secretions throughout the menstrual cycle. Cervical immune barriers fall around ovulation presumably to provide a receptive environment for spermatozoa [7]. Unlike a previous cross-sectional study of adolescents [3], this longitudinal analysis demonstrated that IgA levels decreased during the follicular phase, reached a low at ovulation, and increased
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Cited by (39)
Influence of female sex hormones on proactive behavioral and physiological immune parameters
2024, Reproductive BiologyMucosal immunology of the female reproductive tract and its regulation by female sex hormones
2021, Reproductive Immunology: Basic ConceptsDeciphering sex differences in the immune system and depression
2018, Frontiers in NeuroendocrinologyA randomized clinical trial on the effects of progestin contraception in the genital tract of HIV-infected and uninfected women in Lilongwe, Malawi: Addressing evolving research priorities
2017, Contemporary Clinical TrialsCitation Excerpt :The knowledge/understanding of the mechanism by which hormonal contraception may modify sexually transmitted infection (STI) and HIV risk is incomplete. Hormonal contraception may work systemically or locally within the genital tract to alter HIV susceptibility and transmissibility [14–32]. The physiology, cell composition, and immunology of the genital tract, a critical portal for HIV entry and source of transmission to partners and to newborns during childbirth, can be altered by changes in endogenous hormones and hormonal contraception.
Characterization of cytological changes, IgA, IgG and IL-8 levels and pH value in the vagina of prepubertal and sexually mature Ellegaard Göttingen minipigs during an estrous cycle
2016, Developmental and Comparative ImmunologyCitation Excerpt :In women, the function of both the innate and the adaptive genital immune systems fluctuate during a menstrual cycle due to their strict regulation by sex hormones (Hickey et al., 2011; Weissenbacher, 2014). Within the innate immune system e.g. the level of IL-8 fluctuates through the reproductive cycle (Keller et al., 2007; Shrier et al., 2003) and within the adaptive immune system the genital antibody levels fluctuate. In terms of antibodies, both the levels of total IgG and IgA and the levels of antigen specific IgG and IgA antibodies decrease significantly around ovulation (Keller et al., 2007; Kutteh et al., 1996; Nardelli-Haefliger et al., 2003; Usala et al., 1989; Wright, 2011).
Medroxyprogesterone acetate differentially regulates interleukin (IL)-12 and IL-10 in a human ectocervical epithelial cell line in a glucocorticoid receptor (GR)-dependent manner
2014, Journal of Biological ChemistryCitation Excerpt :However, evidence for the effects of these ligands on IL-10 gene expression is contradictory. Some studies show no effect (79, 82, 83), whereas others are in agreement with the classical mechanism showing an increase in IL-10 mRNA and protein expression (67, 79, 84–86), and some deviate from the classical mechanism by showing a decrease in IL-10 mRNA and protein levels (79, 87–90). Clearly, our results in the ectocervical epithelial cell line showing pro-inflammatory GR-mediated effects by P4, MPA, and cortisol via a unique tethering mechanism deviate from the classically accepted GR mechanism.
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This research was supported in part by 5 K23 MH01845 Mentored Patient-Oriented Research Career Development Award (L.A.S.) from the National Institute of Mental Health and R29 HD33210 (P.A.C.-N.) from the National Institute of Child Health and Development, National Institutes of Health, Bethesda, MD.