Abstract
Preterm labor (PTL) is the most common cause of neonatal death and long-term adverse outcome. The pharmacological agents for PTL prevention are palliative and frequently fail to prevent PTL and improve neonatal outcome. It is essential to fully understand the molecular mechanisms of PTL in order to develop novel therapeutic methods against PTL. Several lines of evidence indicate some chemokines are expressed in gestational tissues during labor or PTL. To reveal the pathophysiological roles of the CX3CL1-CX3CR1 axis in PTL, we performed present study using LPS-induced PTL mice model in CX3CR1-deficient (Cx3cr1-/-) mice. We indicated that PTL was suppressed in Cx3cr1-/- mice and immunoneutralization of CX3CL1 in WT mice. From immunohistochemical and the gene expression analyses, the CX3CL1-CX3CR1 axis has detrimental roles in PTL through intrauterine recruitment of macrophages and the enhancement of macrophage-derived inflammatory mediators. Thus, the CX3CL1-CX3CR1 axis may be a good molecular target for preventing PTL.
Highlights
Preterm labor (PTL) is defined as labor arising from premature uterine contractility and occurs prior to 37 weeks of gestation in human
We demonstrated that the lack of CX3CR1 attenuated LPS-induced PTL, along with the reduction in intrauterine macrophage recruitment, inflammatory cytokine production, and expression of prostaglandin-endoperoxide synthase 2 (PTGS2), known as COX-2
Serum CX3CL1 levels were not increased in term labor with spontaneous labor (TIL) and term labor without spontaneous labor (TNL), compared with preterm control group, indicating that labor itself cannot increase serum CX3CL1 levels (Fig 1A)
Summary
Preterm labor (PTL) is defined as labor arising from premature uterine contractility and occurs prior to 37 weeks of gestation in human. In the United States, approximately 11% of all births are diagnosed as preterm [1], and 15 million premature babies are estimated to be born annually worldwide as a result of PTL. PTL is the most common cause of neonatal death and can cause long-term damages to the brain, bowel, lungs, and eyes, leading to severe lifetime handicap development [2]. PTL remains the biggest problem in obstetrics [3]. PTL prevention is attempted by the administration of pharmacological agents including adrenoreceptor agonists, cyclooxygenase inhibitors, magnesium sulphate, calciumchannel blockers and/or oxytocin antagonists in order to arrest or decrease premature uterine.
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