脂多糖诱发同基因妊娠BALB-c及NOD-SCID小鼠早产模型.docVIP

脂多糖诱发同基因妊娠BALB/c及NOD/SCID小鼠早产模型 　 作者：林羿, 刘兆宇, 狄静芳, 曾耀英 毕业论文 【关键词】; 免疫缺陷;,妊娠耐受;,早产;,啮齿动物模型 毕业论文 　　Premature delivery induced by LPS in syngenetically impregnated BALB/c and NOD/SCID mice 毕业论文 　　　[Abstract]; AIM: To extend understanding of the mechanism of lipopolysaccharide (LPS)induced preterm delivery in syngenetically impregnated BALB/c and NOD/SCID (nonobese diabetic/severe combined immunodeficiency) mice. METHODS: Strategies of LPS stimulation were pursued with or without previous Tolllike receptor 4 (TLR4) blocking. The incidence of LPSinduced preterm delivery and fetal death were compared between the BALB/c and NOD/SCID groups. Guided by the time when all expected preterm deliveries have occurred in the first experiment (i.e., day 16 of gestation), the LPSstimulated mice, with or without previous TLR4 blocking, were killed at the beginning of preterm labor and pooled placentas were collected in each mouse in the second experiment. The expression of cell surface TLR4, CD80, and intracellular TNFα in placenta CD45+ cell population was determined by flow cytometry(FCM). RESULTS: It displayed that preterm delivery could be induced by LPS in BALB/c mice, while the NOD/SCID mice seemed to be resistant to LPS induction. Upon LPS stimulation, TLR4 expression was not changed either in BALB/c or in NOD/SCID mice, but the CD45+CD80+ cell percentage was elevated in both groups. However, the CD45+TNFα+ cell percentage was increased merely in BALB/c mice after stimulation, while no such trend was observed in NOD/SCID mice. In BALB/c mice, the effect of LPS on CD80 and TNFα expression could be abrogated by previous TLR4 blocking, which subsequently prevented LPSinduced preterm delivery. CONCLUSION: Although LPS do not alter TLR4 expression, it interacts with this receptor, triggers the mobilization of CD45+CD80+ cells, results in elevated production of inflammatory cytokines, and finally results in preterm delivery. The diversity of sensitivity to LPS induction ob