Biochemical and biophysical research communications · 2025
Maternal vitamin A deficiency during pregnancy impairs gastrointestinal function and alters the colonic T and B cell immune repertoire in offspring rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gou Lue, Tang Mengxia, Zhou Yi, Li Xiao, Yang Chengxu, Hou Feifei, Chen Yan, Tan Mei
Аннотация
Vitamin A is essential for embryogenesis, immunity, and gut homeostasis. Vitamin A deficiency is a global health issue, particularly in children and women of reproductive age. This study examines how maternal VAD affects offspring rats' gastrointestinal function and colonic T/B cell immunity. Female rats were fed a VAD or VA-normal diet for 5 weeks before mating. Serum retinol levels were measured via HPLC. Offspring were assessed for growth, gut function, and colonic histopathology. RNA sequencing analyzed gene expression, and immune repertoire profiling evaluated T/B cell receptor diversity. Maternal VAD reduced offspring serum VA levels and body weight. VAD offspring showed delayed gut transit, higher fecal water content, colonic inflammation, and fewer goblet cells. Transcriptomics revealed 2020 differentially expressed genes, enriched in immune pathways. VAD suppressed B cell receptor clonal expansion and diversity but increased T cell receptor diversity and clonal expansion. VAD also altered CDR3 sequence features and V/J gene usage. Maternal VAD reshapes offspring colonic immunity by suppressing B-cell responses and enhancing T-cell responses, potentially contributing to gut inflammation. These findings underscore VA's role in gut immunity and suggest maternal VAD may increase offspring susceptibility to gut dysfunction and infections. Further research should explore interventions to mitigate these effects.