Prenatal caffeine ingestion increases susceptibility to pulmonary inflammation in adult female rat offspring

• Published in: Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2017-12, Vol.74, p.212-218
• Main Authors: Liu, Han-xiao, Hou, Li-fang, Chen, Ting, Qu, Wen, Liu, Sha, Yan, Hui-yi, Wen, Xiao, Ping, Jie
• Format: Article
• Language: English
• Subjects: IL-6; IUGR; Prenatal caffeine ingestion; Pulmonary inflammation; Pulmonary interstitial thickness; TNF-α
• ISSN: 0890-6238; 1873-1708
• DOI: 10.1016/j.reprotox.2017.10.006

•PCI increased expression of lung structure-associated genes in offspring.•Upregulation of structural genes contributes to pulmonary interstitial thickness.•Destroyed lung structure results in susceptibility of offspring to inflammation. This study aimed to investigate the association between prenatal caffeine ingestion (PCI) and risk of postnatal pulmonary inflammation. Pregnant Wistar rats were administered 60mg/kg/d caffeine intragastrically from gestational day (GD) 7 to GD 20. The results showed that PCI obviously increased intrauterine growth retardation rate to 39.2% and suppressed weight growth of the offspring. PCI also enhanced the expression of transforming growth factor β, α-smooth muscle actin, interleukin (IL)-1β, and IL-8 in lungs and caused pulmonary interstitial thickening in the offspring. Further, with lipopolysaccharide stimulation on postnatal day 77, PCI offspring showed more serious inflammatory infiltration, higher injury scores, and higher levels of IL-6 and tumor necrosis factor-α in lungs than those of the control. Our findings showed, for the first time, that PCI is a certainly threat to postnatal pulmonary inflammation. The potential mechanism is that PCI alter the expression of pulmonary interstitial thickening-associated genes in the offspring.