{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:26:18Z","timestamp":1791307578668,"version":"4.3.1"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2009,12,1]],"date-time":"2009-12-01T00:00:00Z","timestamp":1259625600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Neurological deficits in children, including cerebral palsy, are associated with prior infection during the perinatal period. Experimentally, we have shown that pre-exposure to the Gram-negative component LPS potentiates hypoxic-ischemic (HI) brain injury in newborn animals. LPS effects are mediated by binding to TLR4, which requires recruitment of the MyD88 adaptor protein or Toll\/IL-1R domain-containing adapter inducing IFN-\u03b2 for signal transduction. In this study, we investigated the role of MyD88 in neonatal brain injury. MyD88 knockout (MyD88 KO) and wild-type mice were subjected to left carotid artery ligation and 10% O2 for 50 min on postnatal day 9. LPS or saline were administered i.p. at 14 h before HI. At 5 days after HI in wild-type mice, LPS in combination with HI caused a significant increase in gray and white matter tissue loss compared with the saline-HI group. By contrast, in the MyD88 KO mice there was no potentiation of brain injury with LPS-HI. MyD88 KO mice exhibited reduced NF\u03baB activation and proinflammatory cytokine-chemokine expression in response to LPS. The number of microglia and caspase-3 activation was increased in the brain of MyD88 KO mice after LPS exposure. Collectively, these findings indicate that MyD88 plays an essential role in LPS-sensitized HI neonatal brain injury, which involves both inflammatory and caspase-dependent pathways.<\/jats:p>","DOI":"10.4049\/jimmunol.0900762","type":"journal-article","created":{"date-parts":[[2009,11,16]],"date-time":"2009-11-16T21:55:14Z","timestamp":1258408514000},"page":"7471-7477","source":"Crossref","is-referenced-by-count":153,"title":["Lipopolysaccharide Sensitizes Neonatal Hypoxic-Ischemic Brain Injury in a MyD88-Dependent Manner"],"prefix":"10.1093","volume":"183","author":[{"given":"Xiaoyang","family":"Wang","sequence":"first","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]},{"name":"Department of Pediatrics, the Third Affiliated Hospital of Zhengzhou University , Zhengzhou,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linnea","family":"Stridh","sequence":"additional","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenli","family":"Li","sequence":"additional","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]},{"name":"Department of Pediatrics, the Third Affiliated Hospital of Zhengzhou University , Zhengzhou,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin","family":"Dean","sequence":"additional","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders","family":"Elmgren","sequence":"additional","affiliation":[{"name":"AstraZeneca Research and Development , M\u00f6lndal,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liming","family":"Gan","sequence":"additional","affiliation":[{"name":"AstraZeneca Research and Development , M\u00f6lndal,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristina","family":"Eriksson","sequence":"additional","affiliation":[{"name":"Department of Rheumatology and Inflammation Research, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Hagberg","sequence":"additional","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]},{"name":"Department of Obstetrics and Gynecology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]},{"name":"Institute of Reproductive and Developmental Biology, Imperial College , London,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carina","family":"Mallard","sequence":"additional","affiliation":[{"name":"Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg , G\u00f6teborg,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2009,12,1]]},"reference":[{"key":"2026012811251843000_R1","first-page":"1","article-title":"Inflammatory brain damage in preterm newborns: dry numbers, wet lab, and causal inferences.","volume-title":"Early Hum. 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