Abstract

BackgroundThe incidence of asthma and obesity continue to rise throughout the world. Past research has shown that obesity can cause numerous complications in asthma patients, including increased severity of symptoms, treatment non‐responsiveness, and required increased dosage of treatments. In addition, maternal obesity has been associated with multiple complications for both the mother and the child, including hypertensive disorders and gestational diabetes for the mother, and macrosomia and congenital abnormalities for the child.We tested the hypothesis that maternal obesity would impair lung growth through the presence of a persistent inflammatory state.MethodsFemale mice were fed high fat diets (HFD) or control diets (CD) for 8 weeks prior to mating and through weaning. Mouse pups were sacrificed at 21 days for inflammation analysis using PCR and western blot. An additional group of mouse pups were placed on CD at weaning and maintained on CD until sacrifice at 3 months. Lungs were inflation fixed and morphometric analyses were performed on H&E stained tissue sections.ResultsAt 3 months, mice exposed to maternal HFD had fewer and larger alveoli than mice exposed to maternal CD. At 21 days, no differences were observed in IL‐6, IL‐5, TNF‐alpha gene expression in lung tissues. There were also no significant differences found in pSMAD 2/3 or IkBa protein levels. There were significantly lower protein levels of p65 and IKKb in HFD mice.ConclusionsMaternal HFD results in decreases in alveolariztion in the offspring. Inflammatory responses and changes in matrix regulation are not evident at 21 days but ongoing chronic inflammation was observed.

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