Abstract

Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies in reproductive-aged women. The pathogenesis of this syndrome is not yet fully understood. Previous studies indicate the coexistence of low-grade chronic inflammation and PCOS. Toll-like receptors (TLRs) play a key role in the inflammatory reactions. They induce an innate immune response when in contact with pathogen-associated molecular patterns (PAMP). TLRs expression on several cell types has been described, including immune cells, epithelial and endothelial cells, adipocytes, pancreatic beta-cells and ovarian tissue. The stimulation of TLRs triggers signaling pathways, which in turn leads to proinflammatory cytokines production, including IL-6 and TNF alpha. Elevated concentrations of these cytokines were also observed in patients with PCOS. Currently, there are few studies about the role of TLRs in the pathogenesis of PCOS. Women with this syndrome are more frequently diagnosed with metabolic disorders, such as obesity or insulin resistance (IR). The substances released from adipose tissue, including free fatty acids, contribute to the increased activation of the two TLRs – 2 and 4. Recent data also confirms their overexpression in women with PCOS. Increased activation and the presence of specific gene polymorphisms for TLR2 and TLR4 is presumed to be a contributor to the development of IR and hyperandrogenism in women with PCOS.

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