Human ICAM1 ELISA Matched Antibody Pair

Preterm birth is the primary cause of neonatal deaths and morbidities. Pathological processes causally linked to preterm birth are inflammation and infection. Pellino-1 (Pelil) has previously been found to regulate the inflammatory response in non-gestational tissues in response to toll-like receptor (TLR) ligands and pro-inflammatory cytokines. The aims of this study were to determine the effect of labor on Pelil expression in myometrium and fetal membranes, and the effect of Pelil silencing by siRNA (siPELI1) on the production of pro inflammatory and pro-labor mediators. The expression of Pelil was found to be higher in myometrium and fetal membranes with term labor, compared to non-laboring samples. Pelil mRNA and protein expression was also higher in amnion from women with preterm histological chorioamnionitis. In human primary myometrial cells, siPELI1 transfected cells showed a decrease in pro-inflammatory cytokine IL6, chemokines (CXCL8, CCL2) and adhesion molecule ICAM1 when in the presence of pro-inflammatory cytokine TNF, TLR2/6 ligand fsl-1, TLR5 ligand flagellin, and TLR3 ligand poly(I:C). Similarly in primary amnion cells, siPELI1 transfected cells decreased IL1B-induced expression and secretion of IL6 and CXCL8. In siPELI1 transfected myometrial cells, there was a decrease in prostaglandin PGF(2 alpha), and its receptor, PTGFR mRNA expression when treated with TNF. There was a decrease in NF-kappa B RELA transcriptional activity in siPELI1 transfected cells in the presence of TNF, fsl-1 and flagellin, but not poly(I:C). Our study suggests a novel role for Pelil in regulating pro-inflammatory and pro labor mediators through TNF and TLR signalling.

Epididymitis is a commonly diagnosed disease associated with male infertility. However, little is known about the molecules that are involved in its development. This study was to identify critical genes associated with lipopolysaccharide-induced epididymitis and analyze the molecular mechanism of epididymitis through RNA sequencing. Experimental epididymitis models were generated by administering male Sprague-Dawley rats' lipopolysaccharide. A total of 1378 differentially expressed genes, including 531 upregulated and 847 downregulated genes, were identified in the epididymitis model rats compared with those in sham-operated rats by RNA sequencing. Functional enrichment analyses suggested that the upregulated genes were markedly enriched in inflammation-related biological processes, as well as in the tumor necrosis factor (TNF) signaling pathway, cytokine-cytokine receptor interactions, complement and coagulation cascades, and in the chemokine signaling pathway. Four downregulated genes (collagen type XXVIII alpha 1 chain [Col28 alpha 1], cyclin-dependent kinase-like 1 [Cdkl1], phosphoserine phosphatase [Psph], and fatty acid desaturase 2 [Fads2]) and ten upregulated genes (CCAAT/enhancer-binding protein beta [Cebp beta], C-X-C motif chemokine receptor 2 [Cxcr2], interleukin 11 [Il11], C-C motif chemokine ligand 20 [Ccl20], nuclear factor-kappa-B inhibitor alpha [Nfkbi alpha], claudin 4 [Cldn4], matrix metallopeptidase 9 [Mmp9], heat shock 70 kDa protein 8 [Hspa8], intercellular cell adhesion molecule-1 [Icam1], and Jun) were successfully confirmed by real-time polymerase chain reaction. Western blot demonstrated that CDKL1 was decreased, while MMP9 and NFKBIA were increased in the experimental model group compared with those in the sham-operated group. Our study sheds new light on the understanding of the early response of the epididymis during bacterial epididymitis.