title: [Premature delivery induced by LPS in syngenetically impregnated BALB/c and NOD/SCID mice].
abstract: OBJECTIVE
  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 Toll-like receptor 4 (TLR4) blocking. The incidence of LPS-induced 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 LPS-stimulated 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 TNF-alpha 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(+) TNF-alpha(+) 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 TNF-alpha expression could be abrogated by previous TLR4 blocking, which subsequently prevented LPS-induced preterm delivery.
  
  
  CONCLUSIONS
  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 observed in BALB/c and NOD/SCID mice implies that the lack of functional T and NK cells in the NOD/SCID may be the reason why the NOD/SCID appeared to be resistant to LPS-induced premature labor.
authors.affiliation: Key Laboratory of Ministry of Education for Tissue Transplantation and Immunology, Jinan University, Guangzhou 510632, China. yilinonline@21cn.com
authors.forename: Yi
authors.initials: Y
authors.lastname: Lin
authors.forename: Zhao-yu
authors.initials: ZY
authors.lastname: Liu
authors.forename: Jing-fang
authors.initials: JF
authors.lastname: Di
authors.forename: Yao-ying
authors.initials: YY
authors.lastname: Zeng
mesh_terms: D000818:Animals; D018122:B7-1 Antigen / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D017493:Leukocyte Common Antigens / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D008807:Mice, Inbred BALB C; D016688:Mice, Inbred NOD; D016513:Mice, SCID; D011247:Pregnancy; D047928:Premature Birth / Q000139:chemically induced* / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000037:antagonists & inhibitors / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018122:B7-1 Antigen; D008070:Lipopolysaccharides; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D017493:Leukocyte Common Antigens