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The physiological processes of labour and birth involve essential roles for immune cells and pro\u2010inflammatory cytokines in gestational tissues. There is compelling evidence that the mechanisms underlying spontaneous preterm birth are initiated when a premature and excessive inflammatory response is triggered by infection or other causes. Exposure to pro\u2010inflammatory mediators is emerging as a major factor in the \u2018fetal inflammatory response syndrome\u2019 that often accompanies preterm birth, where unscheduled effects in fetal tissues interfere with normal development and predispose to neonatal morbidity. Toll\u2010like receptors (TLRs) are critical upstream gatekeepers of inflammatory activation. TLR4 is prominently involved through its ability to sense and integrate signals from a range of microbial and endogenous triggers to provoke and perpetuate inflammation. Preclinical studies have identified TLR4 as an attractive pharmacological target to promote uterine quiescence and protect the fetus from inflammatory injury. Novel small\u2010molecule inhibitors of TLR4 signalling, specifically the non\u2010opioid receptor antagonists (+)\u2010naloxone and (+)\u2010naltrexone, are proving highly effective in animal models for preventing preterm birth induced by bacterial mimetic LPS, heat\u2010killed\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    , or the TLR4\u2010dependent pro\u2010inflammatory lipid, platelet\u2010activating factor (PAF). Here, we summarise the rationale for targeting TLR4 as a master regulator of inflammation in fetal and gestational tissues, and the potential utility of TLR4 antagonists as candidates for preventative and therapeutic application in preterm delivery and fetal inflammatory injury.\n                  <\/jats:p>","DOI":"10.1002\/cti2.1121","type":"journal-article","created":{"date-parts":[[2020,4,14]],"date-time":"2020-04-14T19:55:15Z","timestamp":1586894115000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":64,"title":["Targeting Toll\u2010like receptor\u20104 to tackle preterm birth and fetal inflammatory injury"],"prefix":"10.1002","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9967-0084","authenticated-orcid":false,"given":"Sarah A","family":"Robertson","sequence":"first","affiliation":[{"name":"Robinson Research Institute and Adelaide Medical School University of Adelaide Adelaide SA 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