Correction: Synergic Activation of Toll-Like Receptor (TLR) 2/6 and 9 in Response to Ureaplasma parvum & urealyticum in Human Amniotic Epithelial Cells

Abstract

Ureaplasma species are the most frequently isolated microorganisms inside the amniotic cavity and have been associated with spontaneous abortion, chorioamnionitis, premature rupture of the membranes (PROM), preterm labour (PL) pneumonia in neonates and bronchopulmonary dysplasia in neonates. The mechanisms by which Ureaplasmas cause such diseases remain unclear, but it is believed that inappropriate induction of inflammatory responses is involved, triggered by the innate immune system. As part of its mechanism of activation, the innate immune system employs germ-lined encoded receptors, called pattern recognition receptors (PRRs) in order to ''sense'' pathogens. One such family of PRRs are the Toll like receptor family (TLR). In the current study we aimed to elucidate the role of TLRs in Ureaplasma-induced inflammation in human amniotic epithelial cells. Using silencing, as well as human embryonic kidney (HEK) transfected cell lines, we demonstrate that TLR2, TLR6 and TLR9 are involved in the inflammatory responses against Ureaplasma parvum and urealyticum serovars. Ureaplasma lipoproteins, such as Multiple Banded antigen (MBA), trigger responses via TLR2/TLR6, whereas the whole bacterium is required for TLR9 activation. No major differences were observed between the different serovars. Cell activation by Ureaplasma parvum and urealyticum seem to require lipid raft function and formation of heterotypic receptor complexes comprising of TLR2 and TLR6 on the cell surface and TLR9 intracellularly.

Ureaplasma Species Multiple Banded Antigen (MBA) Variation Is Associated with the Severity of Inflammation In vivo and In vitro in Human Placentae

“…Others have reported the cytokine responses elicited when: (i) adult human monocytes and term and preterm neonatal cord blood were exposed to low (10 3 color changing units [CCU]) or high doses (10 6 CCU) of U. parvum serovars 3 (Manimtim et al, 2001), (ii) human monocytes (THP-1 cells) were treated with heat-killed U. urealyticum (Li et al, 2000), (iii) THP-1 macrophages were exposed to surface lipoproteins of Ureaplasma urealyticum (Peltier et al, 2007), and (iv) human amniotic epithelial cells were exposed to Ureaplasma spp. serovars 2, 3, and 14 (1 × 10 8 bacteria/mL) (Triantafilou et al, 2013). In each of these in vitro experiments, the production of TNF-α was elevated in response to the ureaplasmas/antigens presented.…”