{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T14:34:53Z","timestamp":1790951693913,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2021,4,17]],"date-time":"2021-04-17T00:00:00Z","timestamp":1618617600000},"content-version":"vor","delay-in-days":106,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Key Young Medical Talents Project of Wuxi Health Planning Commission","award":["QNRC019"],"award-info":[{"award-number":["QNRC019"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:p><jats:italic>Objective<\/jats:italic>. The lipopolysaccharide\u2010 (LPS\u2010) induced acute intestinal dysfunction model has been widely applied in recent years. Here, our aim was to investigate the effect of triggering receptor expressed on myeloid cells\u20101 (TREM1) inhibitor in LPS\u2010induced acute intestinal dysfunction. <jats:italic>Methods<\/jats:italic>. Male rats were randomly assigned into normal (saline injection), model (LPS and saline injection), and LP17 (LPS and LP17 (a synthetic TREM1 inhibitor) injection) groups. The levels of intestinal TREM1 expression were evaluated by immunohistochemistry and western blot. Intestinal permeability and apoptosis were separately assessed by the lactulose\/mannitol (L\/M) ratio and TUNEL assay. The levels of soluble TREM1 (sTREM1), TNF\u2010<jats:italic>\u03b1<\/jats:italic>, IL\u20106, and IL\u20101<jats:italic>\u03b2<\/jats:italic> were measured in the plasma and intestinal tissues by ELISA. The expression levels of NF\u2010<jats:italic>\u03ba<\/jats:italic>B, high\u2010mobility group box 1 (HMGB1), and toll\u2010like receptor 4 (TLR\u20104) were measured with RT\u2010qPCR and western blot. After transfection with si\u2010TREM1 in LPS\u2010induced intestinal epithelium\u20106 (IEC\u20106) cells, p\u2010p65 and p\u2010I<jats:italic>\u03ba<\/jats:italic>B<jats:italic>\u03b1<\/jats:italic> levels were detected by western blot. <jats:italic>Results<\/jats:italic>. LP17\u2010mediated TREM1 inhibition alleviated the intestine tissue damage in rats with LPS\u2010induced acute intestinal dysfunction. LP17 attenuated the LPS\u2010induced increase in sTREM1, TNF\u2010<jats:italic>\u03b1<\/jats:italic>, IL\u20106, and IL\u20101<jats:italic>\u03b2<\/jats:italic> levels in the plasma and intestinal tissues. Furthermore, intestine permeability and epithelial cell apoptosis were ameliorated by LP17. LP17 attenuated the LPS\u2010induced increase in the expression of TREM1, HMGB1, TLR\u20104, and NF\u2010<jats:italic>\u03ba<\/jats:italic>B in the intestine tissues. In vitro, TREM1 knockdown inactivated the NF\u2010<jats:italic>\u03ba<\/jats:italic>B signaling in LPS\u2010induced IEC\u20106 cells. <jats:italic>Conclusion<\/jats:italic>. LP17 could ameliorate LPS\u2010induced acute intestinal dysfunction, which was associated with inhibition of intestinal apoptosis and inflammation response.<\/jats:p>","DOI":"10.1155\/2021\/6635452","type":"journal-article","created":{"date-parts":[[2021,4,17]],"date-time":"2021-04-17T17:50:06Z","timestamp":1618681806000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["TREM1 Blockade Ameliorates Lipopolysaccharide\u2010Induced Acute Intestinal Dysfunction through Inhibiting Intestinal Apoptosis and Inflammation 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