ArticleTissue barriers2025
Lipopolysaccharide transport during long-chain fatty acid exposure is mediated by caveolin-1 dependent endocytosis in murine jejunum.
Article in Tissue barriers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Elevated Serum LPS in Newly Diagnosed Hashimoto's Thyroiditis: A Case-Control Study in Bulgaria.Clinics and practice · 2026Article
- Luminal LPS is transported across murine small intestine by a caveolin-1 dependent endocytic mechanism induced by chronic feeding of a Western-style diet.Gut microbes · 2025Article
Corrections and comments
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Authors and funding
5 authors.
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Abstract
The entry of bacterial-derived lipopolysaccharides (LPS) from the intestinal lumen to the circulation induces low-grade systemic inflammation. We have found that LPS is transcellularly transported to the portal vein during luminal long-chain fatty acid (LCFA) exposure via CD36- and lipid raft-mediated pathways in rat jejunum, consistent with the involvement of caveolae-mediated endocytosis. We thus examined LPS transport in wild-type (WT) and caveolin-1 (Cav1) knockout (KO) murine jejunum. FITC-LPS was added to the mucosal bath of Ussing chambered muscle-stripped jejunal mucosa of WT and Cav1KO mice. Serosal appearance of FITC-LPS was measured with or without luminal application of oleic acid (OA, 10 mM) with taurocholic acid (TCA, 0.1 mM), or medium-chain fatty acid (MCFA) sodium caprate (C10, 30 mM). Luminal application of OA/TCA increased FITC-LPS m-to-s transport in WT jejunum, inhibited by the CD36 inhibitor sulfosuccinimidyl oleate or lipid raft inhibitor methyl-β-cyclodextrin, though not by the clathrin inhibitor chlorpromazine or Pitstop2, suggesting that LCFA-induced LPS transport is mediated by caveolae-mediated endocytosis. In contrast, OA/TCA-induced FITC-LPS transport was abolished in Cav1KO jejunum. Nevertheless, luminal C10 increased FITC-LPS transport in both WT and Cav1KO jejuna without transepithelial electrical resistance changes. Chlorpromazine and Pitstop2 inhibited C10-induced FITC-LPS transport, suggesting that C10 enhances transcellular LPS transport via clathrin-mediated endocytosis in the jejunum. These results suggest that LPS transport during LCFA exposure is mediated by Cav1-mediated endocytosis, whereas MCFA-induced LPS transport is via clathrin-mediated endocytosis. Modulation of epithelial endocytosis may be a new therapeutic target for the prevention of dietary lipid -associated endotoxemia, including the metabolic syndrome.
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