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                <title level="j">Journal of Crohn's and Colitis</title>
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                  <biblScope unit="volume">12</biblScope>
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                <term xml:lang="en">inflammatory bowel disease</term>
                <term xml:lang="en">innovative therapy</term>
                <term xml:lang="en">LR12 peptide</term>
                <term xml:lang="en">Animal models of IBD</term>
                <term xml:lang="en">autophagy</term>
                <term xml:lang="en">TREM-1</term>
                <term xml:lang="en">inflammation</term>
                <term xml:lang="en">endoscopy</term>
                <term xml:lang="en">endoplasmic reticulum stress</term>
                <term xml:lang="en">peptide-based therapy</term>
                <term xml:lang="en">dysbiosis</term>
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              <p>Background and Aims: Triggering receptor expressed on myeloid cells-1 [TREM-1] is known to amplify inflammation in several diseases. Autophagy and endoplasmic reticulum [ER] stress, which activate the unfolded protein response [UPR], are closely linked and defects in these pathways contribute to the pathogenesis of inflammatory bowel disease [IBD]. Both autophagy and UPR are deeply involved in host-microbiota interactions for the clearance of intracellular pathogens, thus contributing to dysbiosis. We investigated whether inhibition of TREM-1 would prevent aberrant inflammation by modulating autophagy and ER stress and preventing dysbiosis.Methods: An experimental mouse model of colitis was established by dextran sulphate sodium treatment. TREM-1 was inhibited, either pharmacologically by LR12 peptide or genetically with Trem-1 knock-out [KO] mice. Colon tissues and faecal pellets of control and colitic mice were used. Levels of macroautophagy, chaperone-mediated autophagy [CMA], and UPR proteins were evaluated by western blotting. The composition of the intestinal microbiota was assessed by MiSeq sequencing in both LR12-treated and KO animals.Results: We confirmed that inhibition of TREM-1 attenuates the severity of colitis clinically, endoscopically and histologically. We observed an increase in macroautophagy [ATG1/ULK-1, ATG13, ATG5, ATG16L1, and MAP1LC3-I/II] and in CMA [HSPA8 and HSP90AA1], whereas there was a decrease in the UPR [PERK, IRE-1α, and ATF-6α] protein expression levels in TREM-1 inhibited colitic mice. TREM-1 inhibition prevented dysbiosis.Conclusions: TREM-1 may represent a novel drug target for the treatment of IBD, by modulating autophagy activity and ER stress.</p>
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