![]() Serum levels of female reproductive hormones and oxidative stress biomarkers were estimated in infertile Chlamydia positive women (tubal infertility), fertile Chlamydia positive women and fertile Chlamydia negative women to determine their possible contribution to tubal occlusion in genital Chlamydial infection. Understanding the role of sex steroids in genital Chlamydial infection may be important in preventing the development of sequelae. The mechanisms by which sex steroids orchestrate the balance between reproduction and protection against pathogenic microorganisms, however, are poorly understood. Studies using animal models of genital tract Chlamydial infection suggest that the hormonal status of the genital tract epithelium at the time of exposure may influence the outcome of infection ( 20). The female sex hormones have been reported to exert a number of effects on the immunity and clinical outcome of Chlamydial infections of the female genital tract ( 19). Biomarkers of oxidative stress have been localized in various sites of female reproductive tract ( 18) and elevated ROS levels have been demonstrated in idiopathic infertility ( 16). Postulated pathologic mechanisms include oxidative DNA damage, lipid peroxidation, modulation of gene expression and transcription factors, inhibition of protein synthesis, and depletion of ATP ( 17). It has been implicated in the pathophysiology of tubal factor infertility, endometriosis, preeclampsia, free radical induced birth defects and abortions ( 13– 16). ![]() Oxidative stress precipitates a range of pathologic changes that affect the reproductive functions in both men and women ( 12). Production of ROS in excess of antioxidants results in oxidative stress. Inflammatory response to genital Chlamydia infection leads to activation of polymorphonuclear leukocytes and macrophages resulting in increased production of reactive oxygen species (ROS) ( 11). ![]() In all cases, however, the pathology seems to be related to a chronic inflammation caused by host immune response to chronic persistent Chlamydial infection or frequent reinfections with the bacterium ( 10). However, factors such as human genetics ( 2) and endocrinology ( 3), cytokine profile ( 4), previous infections ( 5), pathogen load ( 6, 7), Chlamydial strain, presence of other genital infections ( 1, 7), route of infection ( 8), oxidative stress and pathologic immune responses to the bacterium have been implicated ( 9). The exact pathologic mechanism of Chlamydial induced tubal damage has not been elucidated. It has been described as potentially, the major cause of tubal occlusion and tubal infertility in women ( 1). Genital Chlamydia infection is considered the most prevalent sexually transmitted bacterial infection throughout the world.
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