Toll-like receptor-4 pathway is required for the pathogenesis of human chronic endometritis.

摘要: Toll-like receptor (TLR) signal transduction is a central component of the primary innate immune response to pathogenic challenge. TLR4, member TLR family, highly expressed in endometrial cells uterus and could thus be key link between human chronic endometritis (CE) system. However, exact biological function TLR4 CE remains largely unexplored. The present study aimed examine role CE. A comprehensive expression activation analysis from patients with (n=25) normal (NE) tissue (n=15) was performed. Western blot analyses demonstrated that compared NE, protein markedly increased Endometrial scrapings were also used for total RNA extraction transcribed amplified by reverse transcription quantitative polymerase chain reaction. results showed significant upregulation tumor necrosis factor-α (TNF-α) interleukin-1β (IL-1β), downregulation IL-10 mRNA observed NE group. Furthermore, signaling adapter myeloid differentiation factor-88 accessory molecules (TNF associated factor 6 transforming growth factor-β-activated kinase 1) detected all assayed tissues. Of note, differential (CE versus NE) immunoblotting at each level nuclear factor-κB cascade, including inhibitor κBα P65 (all P<0.05). altered its corresponding downstream may relevance progression These findings indicate evaluation patterns holds promise treatment