XXXX model: maternal administration of stem cells for prevention of prematurity.

@entity1 @entity32 @entity1545 @entity19 @entity1618 @entity600 @entity777 @entity51 @entity58 @entity2359
OBJECTIVE: Using a @entity19 model of intrauterine @entity32 , we have demonstrated that exposure to @entity32 induces @entity600 and perinatal @entity1545 . Mesenchymal stem cells (MSCs) have been shown to exhibit immunomodulatory effects in many inflammatory conditions. We hypothesized that treatment with @entity1 adipose tissue-derived MSCs may decrease the rate of @entity600 and perinatal @entity1545 through changes in antiinflammatory and regulatory milieu. STUDY DESIGN: A @entity19 model of intrauterine @entity32 was used with the following groups: (1) control; (2) intrauterine @entity32 (lipopolysaccharide); and (3) intrauterine lipopolysaccharide+intraperitoneal (MSCs). Preterm birth was investigated. Luminex multiplex enzyme-linked immunosorbent assays were performed for protein levels of cytokines in maternal and fetal compartments. Immunofluorescent staining was used to identify and localize MSCs and to examine microglial morphologic condition and @entity2359 in perinatal brain. Behavioral testing was performed at postnatal day 5. RESULTS: Pretreatment with MSCs significantly decreased the rate of @entity600 by 21% compared with the lipopolysaccharide group (P<.01). Pretreatment was associated with increased @entity1618 in maternal serum, increased @entity58 in placenta, decreased @entity777 in fetal brain (P<.05), decreased microglial activation (P<.05), and @entity2359 (P<.05). These findings were associated with improved neurobehavioral testing at postnatal day 5 (P<.05). Injected MSCs were localized to placenta. CONCLUSION: Maternally administered MSCs appear to modulate maternal and fetal immune response to intrauterine @entity32 in the model and @entity600 , perinatal @entity1545 , and @entity51 in offspring @entity19 .
