Rocha Martin Vanesa Natalin, Del'Homme Christophe, Chassard Christophe, Schwab Clarissa, Braegger Christian, Bernalier-Donadille Annick, Lacroix Christophe
Laboratory of Food Biotechnology, Department of Health Sciences and Technology, Institute of Food, Nutrition and Health, ETH-Zurich, Zurich, Switzerland.
Division of Gastroenterology and Nutrition, University Children's Hospital Zurich, Zurich, Switzerland.
Front Nutr. 2022 Aug 22;9:902159. doi: 10.3389/fnut.2022.902159. eCollection 2022.
Establishing the relationship between gut microbiota and host health has become a main target of research in the last decade. Human gut microbiota-associated animal models represent one alternative to human research, allowing for intervention studies to investigate causality. Recent cohort and studies proposed an altered gut microbiota and lactate metabolism with excessive H production as the main causes of infant colic. To evaluate H production by infant gut microbiota and to test modulation of gut colonizer lactose- and lactate-utilizer non-H-producer, P279, we established and validated a gnotobiotic model using young germ-free rats inoculated with fecal slurries from infants younger than 3 months. Here, we show that infant microbiota-associated (IMA) rats inoculated with fresh feces from healthy ( = 2) and colic infants ( = 2) and fed infant formula acquired and maintained similar quantitative and qualitative fecal microbiota composition compared to the individual donor's profile. We observed that IMA rats excreted high levels of H, which were linked to a high abundance of lactate-utilizer H-producer . Supplementation of P279 to colic IMA rats reduced H levels compared to animals receiving a placebo. Taken together, we report high H production by infant gut microbiota, which might be a contributing factor for infant colic, and suggest the potential of P279 in reducing the abdominal H production, bloating, and pain associated with excessive crying in colic infants.
在过去十年中，建立肠道微生物群与宿主健康之间的关系已成为研究的主要目标。人类肠道微生物群相关动物模型是人体研究的一种替代方法，可用于进行干预研究以探究因果关系。最近的队列研究和其他研究提出，肠道微生物群改变和乳酸代谢以及过量产氢是婴儿腹绞痛的主要原因。为了评估婴儿肠道微生物群的产氢情况，并测试对肠道定植菌中乳糖和乳酸利用菌（非产氢菌）P279的调节作用，我们使用接种了3个月以下婴儿粪便悬液的无菌幼鼠建立并验证了一种悉生动物模型。在此，我们表明，接种健康婴儿（n = 2）和腹绞痛婴儿（n = 2）新鲜粪便并喂食婴儿配方奶粉的婴儿微生物群相关（IMA）大鼠，与个体供体的情况相比，获得并维持了相似的粪便微生物群数量和质量组成。我们观察到，IMA大鼠排泄出高水平的氢气，这与乳酸利用菌产氢菌的高丰度有关。与接受安慰剂的动物相比，向腹绞痛IMA大鼠补充P279可降低氢气水平。综上所述，我们报告婴儿肠道微生物群产氢量高，这可能是婴儿腹绞痛的一个促成因素，并表明P279在降低腹绞痛婴儿腹部产氢、腹胀和与过度哭闹相关疼痛方面的潜力。
