Hung Chen-Ting, Kern Justin, Trsan Tihana, Panda Santosh K, Laury Marie, Jain Umang, Colonna Marco, Stappenbeck Thaddeus S, Liu Ta-Chiang
Department of Pathology and Immunology, Washington University, Saint Louis, Missouri, USA.
Department of Genetics, Washington University, Saint Louis, Missouri, USA.
FASEB J. 2025 Jun 15;39(11):e70678. doi: 10.1096/fj.202500542R.
The prevalence of obesity in the United States has continued to increase over the past several decades. A growing concern is that transgenerational effects of obesity negatively impact physiologic functions. We showed that consumption of a high fat, high sugar "Western" diet (WD) decreased the density of both gut innate (Paneth cells) and adaptive immune cells (intraepithelial lymphocytes; IEL). We asked whether consumption of WD impacts gut mucosal immunity in the offspring. WD-mediated Paneth cell loss was reversible, whereas IEL loss was not. However, the overall composition of the fecal microbiome and response to infection were defined by the diet consumed by the progeny. Therefore, offspring from obese dams can prevent gut immunity impairment by consuming a healthy diet.
在过去几十年中，美国肥胖症的患病率持续上升。一个日益令人担忧的问题是，肥胖症的跨代效应会对生理功能产生负面影响。我们发现，食用高脂肪、高糖的“西方”饮食（WD）会降低肠道固有免疫细胞（潘氏细胞）和适应性免疫细胞（上皮内淋巴细胞；IEL）的密度。我们询问食用WD是否会影响后代的肠道黏膜免疫。WD介导的潘氏细胞损失是可逆的，而IEL损失则不可逆。然而，粪便微生物群的总体组成和对感染的反应是由后代所食用的饮食决定的。因此，肥胖母鼠的后代可以通过食用健康饮食来预防肠道免疫损伤。
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