Abstract
[This corrects the article DOI: 10.1371/journal.pone.0061199.].
Highlights
Intrauterine infection is a major cause of spontaneous preterm birth (PTB)
Human amniotic epithelial cells were incubated with Ureaplasma SV2, serovar 3 (SV3), and SV14 for different time points and the supernatants were assayed for inflammatory cytokines
Since we demonstrated that Ureaplasma-induced cellular activation is mediated mainly through TLR2 on the cell surface, we proceeded to determine whether TLR2 was recruited within lipid rafts upon stimulation by different Ureaplasma serovars or Multiple Banded antigen (MBA)
Summary
Intrauterine infection is a major cause of spontaneous preterm birth (PTB). There is accumulating epidemiologic and experimental evidence that intrauterine or postnatal infection with Ureaplasma species is a significant risk factor for adverse pregnancy outcomes and complications of extreme preterm birth such as bronchopulmonary dysplasia and intraventricular hemorrhage [1]. Ureaplasma infection is a major risk factor for spontaneous premature rupture of membranes (PROM), clinical chorioamnionitis and preterm delivery [2;3]. It is believed that the innate immune response to these bacteria can lead to the activation of pattern recognition receptors (PRRs), production and release of pro-inflammatory mediators leading to the complications associated with preterm and term infants. Increased levels of pro-inflammatory mediators such as interleukin-6 (IL-6), tumour-necrosis-factor (TNF-a), IL-1band IL-8 have been shown in amniotic fluid infected with Ureaplasma, supporting this hypothesis [8]
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