Bacterial lipopolysaccharide inhibits free thiamin uptake along the intestinal tract via interference with membrane expression of thiamin transporters 1 and 2.

IF 5 2区 生物学 Q2 CELL BIOLOGY American journal of physiology. Cell physiology Pub Date : 2024-11-01 Epub Date: 2024-09-09 DOI:10.1152/ajpcell.00570.2024
Selvaraj Anthonymuthu, Subrata Sabui, Kameron Isaiah Manzon, Alaullah Sheikh, James M Fleckenstein, Hamid M Said
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Abstract

This study examined the effect of exposure of small and large intestinal epithelial cells to the bacterial lipopolysaccharide (LPS) on uptake of free form of vitamin B1, i.e., thiamin. The intestinal tract encounters two sources of thiamin: diet and the gut microbiota. Absorption of thiamin in both the small and large intestine occurs via a carrier-mediated process that involves thiamin transporters 1 and 2 (THTR-1 and -2). Complementary in vitro (human duodenal epithelial HuTu-80 cells and human colonic epithelial NCM460 cells), in vivo (mice), and ex vivo (human primary differentiated enteroid and colonoid monolayers) models were used. The results showed that exposure to LPS causes a significant inhibition in carrier-mediated [3H]-thiamin uptake by small and large intestinal epithelia, with no change in the levels of expression of THTR-1 and -2 mRNAs and their total cellular proteins. However, a significant decrease in the fractions of the THTR-1 and -2 proteins that are expressed at the cell membranes of these epithelial cells was observed. These effects of LPS appeared to involve a protein kinase A (PKA) signaling pathway as activating this pathway caused a reversal in the inhibition of thiamin uptake and level of expression of its transporters at the cell membrane. These findings demonstrate that exposure of gut epithelia to LPS (a situation that occurs under different pathological conditions) leads to inhibition in thiamin uptake due to a decrease in level of expression of its transporters at the cell membrane that is likely mediated via a PKA signaling pathway. NEW & NOTEWORTHY This study shows that the exposure of gut epithelial cells to bacterial LPS negatively impact the uptake process of the free form of vitamin B1 (i.e., thiamin). This appears to be mediated via suppression in the level of thiamin transporters 1 and 2 (THTR-1 and -2) expression at the cell membrane and involves a protein kinase A (PKA) signaling pathway.

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细菌脂多糖通过干扰硫胺素转运体-1和-2的膜表达,抑制肠道对游离硫胺素的摄取。
本研究探讨了小肠和大肠上皮细胞暴露于细菌脂多糖(LPS)对游离态维生素B1(即硫胺素)吸收的影响。肠道中的硫胺素有两个来源:饮食和肠道微生物群。小肠和大肠对硫胺素的吸收是通过载体介导的过程进行的,其中涉及硫胺素转运体-1 和-2(THTR-1 和-2)。研究采用了互补的体外(人十二指肠上皮细胞 HuTu-80 和人结肠上皮细胞 NCM460)、体内(小鼠)和体外(人原代分化肠道和结肠单层细胞)模型。结果表明,暴露于 LPS 会显著抑制小肠和大肠上皮在载体介导下摄取[3H]-硫胺素,THTR-1&-2 mRNA 及其细胞总蛋白的表达水平没有变化。然而,在这些上皮细胞的细胞膜上表达的 THTR-1&-2 蛋白质部分却出现了明显的减少。LPS 的这些影响似乎涉及蛋白激酶 A(PKA)信号通路,因为激活该通路会导致硫胺素摄取抑制和硫胺素转运体在细胞膜上的表达水平发生逆转。这些研究结果表明,将肠道上皮暴露于 LPS(在不同病理条件下会出现这种情况)会导致硫胺素摄取受到抑制,原因是细胞膜上硫胺素转运体的表达水平下降,而这很可能是通过 PKA 信号途径介导的。
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来源期刊
CiteScore
9.10
自引率
1.80%
发文量
252
审稿时长
1 months
期刊介绍: The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.
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