{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T03:23:42Z","timestamp":1784604222475,"version":"3.55.0"},"reference-count":48,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,6,9]],"date-time":"2012-06-09T00:00:00Z","timestamp":1339200000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Molecular Oral Microbiology"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:italic>Campylobacter rectus<\/jats:italic> is associated with fetal exposure and low birthweight in humans. <jats:italic>C. rectus<\/jats:italic> also invades placental tissues and induces fetal intrauterine growth restriction (IUGR) in mice, along with overexpression of Toll\u2010like receptors (TLR4), suggesting that TLR4 may mediate placental immunity and IUGR in mice. To test this hypothesis we examined the effect of <jats:italic>in vitro<\/jats:italic> TLR4 neutralization on trophoblastic proinflammatory activity and studied the IUGR phenotype in a congenic TLR4\u2010mutant mouse strain after <jats:italic>in vivo C.\u00a0rectus<\/jats:italic> infection. Human trophoblasts were pretreated with TLR4 neutralizing antibodies and infected with <jats:italic>C.\u00a0rectus<\/jats:italic>; proinflammatory cytokine production was assessed by cytokine multiplex assays. Neutralizing TLR4 antibodies significantly impaired the production of proinflammatory cytokines in trophoblastic cells after infection in a dose\u2010dependent manner. We used a subcutaneous chamber model to provide a <jats:italic>C.\u00a0rectus<\/jats:italic> challenge in BALB\/cAnPt (TLR4<jats:sup>Lps\u2010d<\/jats:sup>) and wild\u2010type (WT) females. Females were mated with WT or TLR4<jats:sup>Lps\u2010d<\/jats:sup> males once\/week; pregnant mice were infected at (E)7.5 and sacrificed at (E)16.5 to establish IUGR phenotypes. Maternal <jats:italic>C.\u00a0rectus<\/jats:italic> infection significantly decreased fetal weight\/length in infected WT when compared with sham WT controls (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.05, analysis of variance). However, infected TLR4<jats:sup>Lps\u2010d\u2212\/\u2212<\/jats:sup> mice did not show statistically significant differences in fetal weight and length when compared with WT controls (<jats:italic>P<\/jats:italic>\u2003&gt;\u20030.05). Furthermore, heterozygous TLR4<jats:sup>Lps\u2010d+\/\u2212<\/jats:sup> fetuses showed IUGR phenotype rescue. We conclude that TLR4 is an important mediator of trophoblastic proinflammatory responses and TLR4\u2010deficient fetuses do not develop IUGR phenotypes after <jats:italic>C.\u00a0rectus<\/jats:italic> infection, suggesting that placental cytokine activation is likely to be mediated by TLR4 during low birthweight\/preterm birth pathogenesis.<\/jats:p>","DOI":"10.1111\/j.2041-1014.2012.00651.x","type":"journal-article","created":{"date-parts":[[2012,4,16]],"date-time":"2012-04-16T17:00:11Z","timestamp":1334595611000},"page":"373-381","source":"Crossref","is-referenced-by-count":23,"title":["Toll\u2010like receptor 4 mediates intrauterine growth restriction after systemic <i>Campylobacter rectus<\/i> infection in 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