Cytokine expression pattern in the genital tract ofChlamydia trachomatispositive infertile women – implication for T-cell responses

Abstract

SUMMARYHuman genital infection caused by C hlamydia trachomatis is thought to be immunologically mediated, resulting in local recruitment of lymphocyte subsets and inducing the production of cytokines. Little information is available about the role of lymphocyte recruitment and the regulation of cytokine production in the genital tract of C. trachomatis positive infertile women. We have evaluated the recruitment of lymphocyte subsets in the genital tract and production of Th1/Th2 cytokines in cervical secretions and laparoscopic specimens from the fallopian tubes of C. trachomatis positive infertile women ( n = 17) and compared them with controls, viz. C. trachomatis negative infertile women ( n = 20) using ELISA and flow cytometry. None of these patients were found to be infected either with Candida sps., bacterial vaginosis, Trichomonas vaginalis , Neisseria gonorrhoeae, Mycoplasma hominis or Ureaplasma urealyticum in the cervix. Flow cytometric analysis of cervical secretions in Chlamydia positive women revealed recruitment of both CD4 and CD8 lymphocytes to the genital tract was up-regulated and a variation in the production rates of different cytokines in cervical secretions and fallopian tube was observed. We found that the immune responses in cervical secretions were of Th0 type, since all the analysed cytokines, viz. IFN-g , TNF-a , IL-10 and IL-12 were up-regulated. As, both CD4 and CD8 cells contribute to the production of IFN-g and IL-10, these results suggest that along with CD4 cells, CD8 lymphocytes also may be important for local regulation of Th1/Th2 responses in the genital tract during C. trachomatis infection.

Modulation of vaginal immune response among pregnant women with bacterial vaginosis by Trichomonas vaginalis, Chlamydia trachomatis, Neisseria gonorrhoeae, and yeast

“…35 We did not observe an increased proinflammatory response in vaginal fluid associated with BV and N gonorrhoeae infection. Our results concur with observations of other authors about N gonorrhoeae infection at vaginal level.…”

Chlamydial Infection Increases Gonococcal Colonization in a Novel Murine Coinfection Model

“…Two days later, all mice were inoculated with PBS, rather than N. gonorrhoeae. Vaginal levels of seven different cytokines and chemokines (MIP-2, IL-1␤, TNF-␣, IFN-␥, RANTES, IL-10, and IL-17) that were previously implicated in gonococcal (11,22,25,47,58) or chlamydial (5,16,17,63,66,83) infection were measured on the day of PBS challenge and over the next 10 days. Consistent with C. muridarum inducing an inflammatory response, high levels of IFN-␥, TNF-␣, IL-1␤, and MIP-2 were detected in mice that were not treated with estradiol on days 1 to 4 postinoculation.…”

Diagnosis of Chlamydia trachomatis in patients with reactive arthritis and undifferentiated spondyloarthropathy

“…Also, as uSpA is a forme fruste of ReA, and taken together, both ReA as well as uSpA constitute the seronegative spondyloarthropathy group, patients categorized as uSpA by a rheumatologist were also included in the study. Furthermore, despite a high prevalence of genital C. trachomatis in our country [17][18][19][20][21][22][23][24][25], this pathogen appears to be overlooked in seronegative spondyloarthropathies such as ReA and uSpA in India. In order to find the magnitude of the problem, we investigated patients with ReA or uSpA in a case-control study by molecular and nonmolecular methods for the intra-articular presence of C. trachomatis MOMP, plasmid genes, and local or systemic anti-chlamydial IgA or IgG antibodies.…”