Department of Nutrition & Integrative Physiology, Florida State University, Tallahassee, Florida, USA.
Arkansas Children's Nutrition Center, Little Rock, Arkansas, USA; Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
J Nutr Biochem. 2022 Sep;107:109065. doi: 10.1016/j.jnutbio.2022.109065. Epub 2022 May 21.
Enteric infections are widespread in infants and children living in low-resource settings. Iron availability in the gastrointestinal tract may modify the gut microbiome and impact the incidence and severity of enteropathy. This study was designed to determine the effect of an iron-deplete compared to an iron-rich environment in the lower intestine on the gut microbiome, and whether iron availability in the lower intestine affects the host immune response and severity of enteric infection in young mice. Weanling C57BL/6 female mice were fed an iron deficient (Fe, <6 ppm iron) or an iron fortified (Fe, 300 ppm iron) diet for 6 weeks. Mice were pretreated with streptomycin prior to oral inoculation of Salmonella enterica subspecies enterica serovar Typhimurium to induce enteric infection (Sal) or saline control (Sal). Cecal iron concentrations were 55-fold greater with FeSal compared to FeSal. Microbiome sequencing revealed shifts in gut microbiota with dietary iron and enteric infection. There was ∼30% more S. Typhimurium in the cecum of FeSal compared to FeSal. Plasma hepcidin increased with dietary iron and enteric infection, but was greatest in FeSal. Plasma lipocalin-2 and spleen size relative to bodyweight were greater in FeSal compared to FeSal, FeSal and FeSal, and FeSal lost more bodyweight compared to FeSal. Unabsorbed iron in the lower intestine modifies the gut microbiome and promotes a more severe enteropathy. These findings could suggest the need for alternative iron supplementation strategies in areas where enteric infection are common.
肠道感染在资源匮乏环境中生活的婴幼儿中广泛存在。胃肠道中的铁含量可能会改变肠道微生物组，并影响肠道疾病的发病率和严重程度。本研究旨在确定与富含铁的环境相比，铁缺乏的环境（铁含量<6ppm）对下肠道微生物组的影响，以及下肠道的铁含量是否会影响宿主的免疫反应和幼鼠肠道感染的严重程度。我们用缺铁（Fe，<6ppm 铁）或富铁（Fe，300ppm 铁）饮食喂养 6 周龄的 C57BL/6 雌性小鼠。在口服接种鼠伤寒沙门氏菌亚种 Typhimurium 诱导肠道感染（Sal）或生理盐水对照（Sal）之前，用链霉素预处理小鼠。与 FeSal 相比，FeSal 的盲肠铁浓度高 55 倍。微生物组测序显示，饮食铁和肠道感染会导致肠道微生物群发生变化。与 FeSal 相比，FeSal 的盲肠中约有 30%更多的鼠伤寒沙门氏菌。与 FeSal 相比，饮食铁和肠道感染会导致血浆铁调素增加，但在 FeSal 中最高。与 FeSal 相比，FeSal 的血浆脂联素-2 和脾脏重量与体重的比值更大，FeSal 比 FeSal 失去更多的体重。下肠道未被吸收的铁改变了肠道微生物组，并促进了更严重的肠道疾病。这些发现可能表明，在肠道感染较为常见的地区，需要采取替代的铁补充策略。
