ABSTRACT
In recent years, group B streptococcus (GBS) has become an important pathogen that causes infections in many neonatal organs, including the brain, lung, and eye (Ballard et al., 2016). A series of studies performed on GBS infections in western countries have revealed that GBS is one of the primary pathogens implicated in perinatal infection, and GBS infections are a major cause of neonatal morbidity and mortality in the United States (Decheva et al., 2013). In China, GBS is mainly found by screens for adult urogenital tract and perinatal infections, and neonatal GBS infections have been rarely reported. The incidence rate of early-onset neonatal GBS disease is thought to be lower in China than in western countries; however, this data is controversial since it also reflects the clinical interest in GBS (Dabrowska-Szponar and Galinski, 2001).
Subject(s)
Adult , Female , Humans , Pregnancy , Anti-Bacterial Agents/therapeutic use , China/epidemiology , Drug Resistance , Drug Resistance, Bacterial , Incidence , Mothers , Parity , Pregnancy Complications, Infectious/diagnosis , Risk Factors , Streptococcal Infections/drug therapy , Streptococcus agalactiaeABSTRACT
OBJECTIVE@#The purpose of this study was to determine the role of Ureaplasma urealyticum-derived lipid-associated membrane proteins (LAMPs) in the host innate immune system, specifically their effect on Toll-like receptors (TLRs).@*METHODS@#LAMPs were derived from U. urealyticum strains, and human amniotic epithelial cells (HAECs) were isolated from healthy full-term placentas. Cytokine concentrations were determined by enzyme-linked immunosorbent assay (ELISA) and TLR2 mRNA by real-time PCR. Expression of TLR2 was confirmed by Western blotting and immunohistochemistry.@*RESULTS@#LAMPs induced HAECs to produce inflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α. Cytokine production was reduced after blocking TLR2 using TLR2 inhibitor (anti-hTLR2-IgA).@*CONCLUSIONS@#LAMPs isolated from U. urealyticum induced TLR2-dependent up-regulation of inflammatory genes and cytokines in HAECs.