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Polycystic ovary syndrome (PCOS) is a multifaceted syndrome correlated to hyperandrogenism and increased renin-angiotensin system activity (1,2). In other words, PCOS is a heterogeneous disease which results from interactions between genetic, epigenetic, and lifestyle factors (1). This complex endocrine disease can be observed in 5-10% of women who are in their reproductive age throughout the world (1,2). Hyperandrogenism, polycystic ovaries, and chronic anovulation based on Rotterdam criteria are the major diagnostic criteria of PCOS women (3). Further, these patients usually suffer from obesity, insulin resistance, metabolic syndrome, and cardiovascular diseases (4). Recent research recognized PCOS as a chronic lowgrade pro-inflammatory disorder associated with different metabolic and reproductive abnormalities (5). Many circulating inflammatory markers are found to mediate PCOS in response to a stimulus, including pro-inflammatory cytokines and chemokines, as well as different endothelial inflammation markers and oxidative stress and chronic inflammation markers (6). Cytokines involve in the regulation of ovarian function through controlling paracrine or autocrine ovarian processes (7). Furthermore, they control folliculogenesis and ovulation through providing an environment which supports follicle selection and growth. Regarding the folliculogenesis, cytokines regulate the proliferation or differentiation of cells, the survival or atresia of follicles, and oocyte maturation (8). Moreover, an impaired balance between cytokines with inflammatory and anti-inflammatory activities seems to involve in the development of PCOS (9). T helper cell type 2 (Th2) cytokines such as interleukin (IL-3) and IL-5 contribute to inflammatory reactions and immune responses. Additionally, IL-3 secreted from helper lymphocytes, eosinophils, and natural lethal cells affects blood progesterone and mast cells (10, 11). Similarly, IL-3 concentration enhances before delivery during normal pregnancy and progesterone regulates the production of this cytokine via the induction of a specific protein designated as a progesterone-induced blocking factor (12). Likewise, IL-3 and IL-5 regulate the growth, differentiation, and activation of eosinophils under normal physiological conditions. Previous research indicated that the overexpression of IL-5 in the transgenic mice is associated with the increased number of eosinophils in Abstract Objectives: Cytokines regulate ovarian activity through controlling internal ovarian processes as paracrine or autocrine regulators. In the current study, the follicular fluid (FF) concentration of some cytokines including interleukin (IL-3), IL-5, and IL-6 were investigated and compared between 39 patients diagnosed with polycystic ovary syndrome (PCOS) and 34 healthy normal women with male factor infertility as the control group. Materials and Methods: To this end, FF samples were collected by following gonadotropin-releasing hormone antagonist protocol. Then, the FF concentration of the studied cytokines was evaluated using the enzyme-linked immunosorbent assay method. Finally, the characteristics of the participants were collected and compared between PCOS and control groups. Results: Based on the results, the FF concentration of IL-3 and IL-5 revealed a remarkable reduction in the PCOS group in comparison to the control group (P = 0.0004 and P = 0.04, respectively). In addition, there were noticeable differences in the body mass index (P = 0.009), endometrial thickness (P < 0.0001), menstrual cycle (P < 0.0001), history of ovarian surgery (P < 0.0001), hyperandrogenism (P < 0.0001), and hirsutism (P < 0.0001) between the groups. Conclusions: In general, the finding of the diminished concentration of IL-3 and IL-5 in PCOS patients may represent an altered immune response to the inflammatory condition in this syndrome.

A Cross-sectional Study on the Follicular Fluid Concentration of Some Interleukins and Clinical Factors in Polycystic Ovary Syndrome Patients