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Differential fetal exposure to inflammatory assaults in Wistar and Zucker rats
Author(s) -
Palmgren Muriel S.,
Corll Conni,
Svec Frank,
Porter Johnny R.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.807.12
Subject(s) - fetus , gestation , medicine , lipopolysaccharide , amniotic fluid , inflammation , saline , endocrinology , pregnancy , biology , genetics
Periodontal disease has been linked to cardiovascular disease and preterm birth in humans. Oral inflammation is thought to accelerate inflammation at other sites. An animal model is needed to test this hypothesis. We propose that the intensity of inflammatory response in different strains of rats affects the fetus differently. If so, such differences might explain differences seen in studies of humans. We injected pregnant Wistar (W) and Zucker (Z) rats with 1 mg/kg of lipopolysaccharide (LPS) or saline on gestation day 18. Serum and amniotic fluid (AF) were collected 4 hours later. Saline‐injected rats had no response. Zucker rats had higher TNFα (serum=71,977 pg/ml; AF=161pg/ml) and IL‐6 (serum>200,000 pg/ml; AF=1,985 pg/ml) than Wistar rats (TNFα: Serum=599 pg/ml; AF<15 pg/ml; IL‐6: Serum=22,778 pg/ml; AF<15 pg/ml). Zucker rats died or were moribund by 4 hours. Gestation was not shortened in LPS‐treated Wistar rats. The Zucker fetus was exposed to cytokines at 4 hours post‐injection while the Wistar fetus was not. The Zucker rat is a better model for inflammatory assaults on the fetus. Supported in part by Research Grant No. 21‐FY1251 from the March of Dimes Birth Defects Foundation.