Sato Hirokazu, Zhang Linda S, Martinez Kristina, Chang Eugene B, Yang Qing, Wang Fei, Howles Philip N, Hokari Ryota, Miura Soichiro, Tso Patrick
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Gastroenterology. 2016 Nov;151(5):923-932. doi: 10.1053/j.gastro.2016.07.009. Epub 2016 Jul 18.
BACKGROUND & AIMS: The gut microbiota affects intestinal permeability and mucosal mast cells (MMCs) responses. Activation of MMCs has been associated with absorption of dietary fat. We investigated whether the gut microbiota contributes to the fat-induced activation of MMCs in rats, and how antibiotics might affect this process.
Adult male Sprague-Dawley rats were given streptomycin and penicillin for 4 days (n = 6-8) to reduce the abundance of their gut flora, or normal drinking water (controls, n = 6-8). They underwent lymph fistula surgery and after an overnight recovery were given an intraduodenal bolus of intralipid. We collected intestinal tissues and lymph fluid and assessed activation of MMCs, intestinal permeability, and fat transport parameters.
Compared with controls, intestinal lymph from rats given antibiotics had reduced levels of mucosal mast cell protease II (produced by MMCs) and decreased activity of diamine oxidase (produced by enterocytes) (P < .05). Rats given antibiotics had reduced intestinal permeability in response to dietary lipid compared with controls (P < .01). Unexpectedly, antibiotics also reduced lymphatic transport of triacylglycerol and phospholipid (P < .01), concomitant with decreased levels of mucosal apolipoproteins B, A-I, and A-IV (P < .01). No differences were found in intestinal motility or luminal pancreatic lipase activity between rats given antibiotics and controls. These effects were not seen with an acute dose of antibiotics or 4 weeks after the antibiotic regimen ended.
The intestinal microbiota appears to activate MMCs after the ingestion of fat in rats; this contributes to fat-induced intestinal permeability. We found that the gut microbiome promotes absorption of lipid, probably by intestinal production of apolipoproteins and secretion of chylomicrons.
肠道微生物群会影响肠道通透性和黏膜肥大细胞(MMCs)反应。MMCs的激活与膳食脂肪的吸收有关。我们研究了肠道微生物群是否会导致大鼠脂肪诱导的MMCs激活,以及抗生素如何影响这一过程。
成年雄性Sprague-Dawley大鼠连续4天给予链霉素和青霉素(n = 6 - 8)以减少其肠道菌群数量,或给予正常饮用水(对照组,n = 6 - 8)。它们接受了淋巴瘘手术,过夜恢复后给予十二指肠内脂质乳剂推注。我们收集肠道组织和淋巴液,并评估MMCs的激活、肠道通透性和脂肪转运参数。
与对照组相比,给予抗生素的大鼠肠道淋巴液中黏膜肥大细胞蛋白酶II(由MMCs产生)水平降低,二胺氧化酶(由肠上皮细胞产生)活性降低(P < 0.05)。与对照组相比,给予抗生素的大鼠对膳食脂质的肠道通透性降低(P < 0.01)。出乎意料的是,抗生素还减少了三酰甘油和磷脂的淋巴转运(P < 0.01),同时黏膜载脂蛋白B、A-I和A-IV水平降低(P < 0.01)。给予抗生素的大鼠与对照组在肠道蠕动或肠腔胰脂肪酶活性方面未发现差异。急性剂量的抗生素或抗生素治疗结束4周后未观察到这些效应。
肠道微生物群似乎在大鼠摄入脂肪后激活MMCs;这有助于脂肪诱导的肠道通透性增加。我们发现肠道微生物群促进脂质吸收,可能是通过肠道产生载脂蛋白和分泌乳糜微粒实现的。