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Small intestinal inflammation shapes the transcriptomic signature of incoming monocytes in a partially Trem1-dependent mechanism

ABSTRACT: In this study we showed that Trem1 is one of genes that were differentially regulated in donor monocytes recovered from non-inflamed and inflamed small intestine of recipient mice. We, therefore, aimed at investigating the role of Trem1 on regulating the monocyte adapatation and differentiation in a context-dependent manner. Thus, the gene expression of WT and Trem1-deficient donor monocytes that are recruited to non-inflamed and inflamed small intestine one day after transfer.

ORGANISM(S): Mus musculus

PROVIDER: GSE132549 | GEO | 2019/06/12

REPOSITORIES: GEO

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Small intestinal inflammation shapes the transcriptomic signature of incoming monocytes in a partially Trem1-dependent mechanism

Project description:Small intestinal inflammation shapes the transcriptomic signature of incoming monocytes in a partially Trem1-dependent mechanism

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Project description:TREM-1 is an orphan immunoreceptor expressed on monocytes, macrophages, and neutrophils. TREM-1 associates with and signals via the adapter protein DAP12/TYROBP, which contains an immunoreceptor tyrosine-based activation motif (ITAM). TREM-1 activation by receptor cross-linking is pro-inflammatory, and can amplify cellular responses to Toll-like receptor (TLR) ligands such as bacterial lipopolysaccharide (LPS). To investigate the cellular consequences of TREM-1 activation, we have characterized global gene expression changes in human monocytes in response to TREM-1 cross-linking in comparison to and combined with LPS. Both TREM-1 activation and LPS up-regulate chemokines, cytokines, matrix metalloproteases, and PTGS/COX2, consistent with a core inflammatory response. However, other immunomodulatory factors are selectively induced, including SPP1 and CSF1 (i.e., M-CSF) by TREM-1 activation and IL-23 and CSF3 (i.e., G-CSF) by LPS. Additionally, cross-talk between TREM-1 activation and LPS occurs on multiple levels. While synergy in GM-CSF protein production is reflected in commensurate mRNA abundance, comparable synergy in IL-1b protein production is not. TREM-1 activation also attenuates the induction of some LPS target genes, including those that encode IL-12 cytokine family subunits. Whereas positive TREM-1 outputs are abolished by the PI3K inhibitor wortmannin, this attenuation is largely PI3K-independent. These experiments provide a detailed analysis of the cellular consequences of TREM-1 activation, and highlight some of the complexity in signal integration between ITAM- and TLR-mediated signaling. Experiment Overall Design: 11 anonymous donors were treated with Vehicle, isotype control antibody, TREM1 antibody, LPS, isotype control antibody plus LPS and TREM1 antibody plus LPS

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