Please use this identifier to cite or link to this item: http://adhlui.com.ui.edu.ng/jspui/handle/123456789/186
Title: CYTOKINES, REPRODUCTIVE HORMONES AND OXIDATIVE STRESS INDICES IN GENITAL CHLAMYDIA INFECTION IN NIGERIANS WITH TUBAL INFERTILITY
Authors: NSONWU, A. C.
Keywords: Chlamydia trachomatis
Reproductive Hormones
Tubal Infertility
Oxidative stress
Issue Date: Nov-2012
Abstract: Tubal damage is the commonest cause of infertility in Nigerians and Genital Chlamydia Infection (GCI) is one of the major causes. Pathologic mechanisms involving hormonal, oxidative and cytokine responses have been suggested to be the cause of GCI-induced tubal damage. This study was designed to identify the effects of GCI on hormonal, oxidative and cytokine responses in Nigerians with tubal infertility. Two hundred consenting women (28 – 38 years) were enrolled consecutively based on their fertility status and Chlamydia trachomatis antibody (CtIgG) positivity from University College Hospital and Adeoyo Maternity Hospital, Ibadan. They were divided into four groups of 50 each: A (fertile women without GCI), B (fertile women with GCI), C (infertile women without GCI) and D (infertile women with GCI). Socio-demographic characteristics and anthropometric indices were obtained. High Vaginal Swabs (HVS) and Endocervical Swabs (ES) were collected for detection of Niesierria gonnorrheae (Ng) and Trichomonas vaginalis (Tv) by microscopy and culture. Chlamydia trachomatis antigen (CtAg) and Treponema pallidium (Tp) antibodies were detected by immunochromatography. Blood (10ml) was collected and serum obtained for analysis of reproductive hormones, oxidative stress biomarkers and cytokines. Chlamydia trachomatis antibody, reproductive hormones [Follicle Stimulating Hormone (FSH), Luteinizing Hormone (LH), Oestradiol (E2), Progesterone (P4), Prolactin (PRL)] and oxidative stress biomarkers [Total Antioxidant Capacity (TAC) and 8-hydroxyl-2-deoxyguanosine (8-OHdG)] were determined by enzyme immunoassay (EIA). Cytokines [Transforming Growth Factor beta 1 (TGFβ1), Interferon Gamma (IFNγ), Tumour Necrosis Factor alpha (TNFα), Interleukin 4 (IL-4), Interleukin 10 (IL-10) and Interleukin 17A (IL-17A)] were assayed by enzyme linked immunosorbent assay (ELISA). Data were analysed using ANOVA and multiple regression to determine differences between means and relationships respectively at p = 0.05. No Ng, Tv, Tp and CtAg in HVS and ES were found in the four groups. Comparison within the infertile groups C and D showed no differences in all indices tested. The TNFα level was significantly lower in group B compared with A. Among women with GCI, significantly higher levels of LH and 8-OHdG, and lower IFNγ were observed in D compared with B. Among women without GCI, LH and 8-OHdG levels were significantly increased while TGFβ1 and IFNγ levels were significantly reduced in C compared with A. Significantly elevated LH, 8-OHdG and reduced TAC and IFNγ levels were observed in D compared with A. In group A, IL-17A (β=0.372) and TNFα (β=0.537) positively predicted TGFβ 1, while TNFα (β=0.424) positively predicted IL-4. In group B, TNFα (β = 0.251), IL-10 (β = 0.220) and IL-17A (β = 0.764) positively predicted TGFβ 1. The IL-17A positively predicted IFNγ and TNFα (β =0.637, β = 0.679) respectively in C. In group D, TGFβ 1 (β =0.668) positively predicted IFNγ, IL-4 (β = 0.918) and IL-10 (β = 0.493) positively predicted TNFα, IL-4 was positively predicted by IL-17A (β = 0.635) and negatively by IL-10 (β =-0.241). Oxidative deoxyribonucleic acid damage and inflammatory mechanisms may be involved in the pathology of tubal infertility in Nigerians. Enhanced total antioxidant capacity and interferon gamma may protect against this pathologic state.
Description: A thesis in the Department of Chemical Pathology Submitted to the Faculty of Basic Medical Sciences in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY of the University of Ibadan, Nigeria.
URI: http://adhlui.com.ui.edu.ng/jspui/handle/123456789/186
Appears in Collections:Theses in Chemical Pathology

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