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. 2018 Sep 19;9:553. doi: 10.3389/fendo.2018.00553

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Copyright © 2018 Lehto and Groop.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Putative interconnections between LPS-detoxification and intestinal barrier function. Intestinal alkaline phosphatase (IAP) detoxifies bacterial lipopolysaccharides (LPS; endotoxins) by dephosphorylation. Butyrate, a short-chain fatty acid produced as a result of bacterial fermentation, stimulates IAP gene expression. IAP may also modulate composition of microbial community via regulation of secretory IgA release. Fecal calprotectin is a commonly used marker for increased neutrophil (NEU) migration and local inflammation in patients with gastrointestinal diseases. Lower luminal IAP-activity may lead to increased production of toxic LPS-molecules, which in turn may stimulate Factor XII regulated contact activation pathway in the gut. Subsequent activation of kallikrein-kinin system by endotoxins may potentiate leakiness of the intestinal wall. Modified from Lassenius et al. (103).