Inflammatory cytokines in a murine model of infection-induced preterm labor: cause or effect?
Inflammatory cytokines in a murine model of infection-induced preterm labor: cause or effect?
复制标题
感染诱发早产的小鼠模型中的炎症细胞因子：原因还是影响？
DOI：
10.1016/s1071-5576(99)00013-1
复制
发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Hirsch,E
中科院分区：
文献类型：
--
作者：
Mussalli,GM;Blanchard,R;Brunnert,SR;Hirsch,E
ObjectiveTo characterize the expression of inflammatory cytokines in a murine model of preterm delivery induced by heat-killed bacteria.MethodsThe right uterine horns of female CD-1 mice on day 14.5 of 19-20 days of gestation were inoculated with either sterile media or killed Excherichia coli bacteria (105-1010organisms per mouse). The incidence of preterm delivery was recorded. The concentrations of cytokines (itnerleukin [IL-] 1α, IL-1β, IL-1 receptor antagonist [IL-1ra], IL-6, and tumor necrosis factor α [TNFα]) within maternal and fetal tissue homogenates were determined by enzyme-linked immunosorbent assay at various times after inoculation.ResultsKilled E. coli induced preterm delivery in a dose-dependent fashion. Inoculation with 1010bacteria (sufficient to cause delivery in all mice) produced increases in IL-1α, IL-1β, IL-6, and TNFα within uteri and fetal membranes, but not within placentas, fetal bodies, and maternal serum. Maximum mean uterine levels of IL-1 and IL-6 exceeded those of fetal tissues (membranes, placentas, and fetal bodies) by greater than 15-fold. Maximal uterine IL-1 and TNFα levels following inoculation with 1010bacteria exceeded those that followed inoculation with 107bacteria (below the threshold for delivery) by 2.5- to 5-fold. The anti-inflammatory cytokine IL-1ra was expressed in higher concentrations in fetal than in maternal tissues and was unaltered by the bacterial inoculum.ConclusionsE. coli induce labor in mice even in the absence of bacterial viability. Although IL-1 and TNFα were upregulated by bacterial inocula causing delivery, peak levels were only 2.5- to 5-fold higher than those that occurred with inocula below the threshold for delivery (1000-fold fewer bacteria). Whether IL-1 and TNFα mediate labor during in vivo infection, or whether the upregulation of these cytokines merely represents an epiphenomenon accompanying infection, remains unknown.
