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- Publisher Website: 10.1186/s12929-019-0539-4
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- PMID: 31189465
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Article: TREM-1-dependent M1 macrophage polarization restores intestinal epithelium damaged by DSS-induced colitis by activating IL-22-producing innate lymphoid cells
Title | TREM-1-dependent M1 macrophage polarization restores intestinal epithelium damaged by DSS-induced colitis by activating IL-22-producing innate lymphoid cells |
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Authors | |
Keywords | Triggering expressed on myeloid cells-1 Group 3 innate lymphoid cells Inflammatory macrophages IL-22 Colitis |
Issue Date | 2019 |
Citation | Journal of Biomedical Science, 2019, v. 26, n. 1, article no. 46 How to Cite? |
Abstract | Background: Triggering receptor expressed on myeloid cells-1 (TREM-1) is highly expressed on macrophages in inflamed intestines and reportedly promotes inflammatory bowel disease (IBD) by augmenting pro-inflammatory responses. To study the mechanism mediated by TREM-1 on macrophages, we generated an independent TREM-1 deficient mouse. Methods: Acute colitis was induced in C57BL/6 and TREM-1-deficient mice by the administration of dextran sodium sulfate (DSS). Colonic lamina propria immune cell composition and cytokines were analyzed. An innate lymphoid cell (ILC) co-culture experiment with macrophages was used to analyze IL-22 levels. Exogenous IL-22 and TREM-1-expressing macrophages were supplied to TREM-1-deficient mice for examining their effects on intestinal barrier integrity. Results: In inflamed colons, TREM-1 loss compromised the activation of ILC3 and their production of IL-22, which is required for intestinal barrier integrity. ILC3-mediated IL-22 production depends on IL-1β secreted by M1-polarized macrophages, and we found that TREM-1 deficiency results in a decreased number of IL-1β producing-M1 macrophages in colons exposed to DSS. Accordingly, DSS-mediated damage was ameliorated by supplying exogenous IL-22 and TREM-1-expressing macrophages to TREM-1-deficient mice. Conclusions: TREM-1 plays a crucial role in regulating IL-22 production by ILC3 through modulating M1-macrophage polarization during DSS-induced acute colitis. |
Persistent Identifier | http://hdl.handle.net/10722/292118 |
ISSN | 2023 Impact Factor: 9.0 2023 SCImago Journal Rankings: 2.606 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Yang, Fu Chen | - |
dc.contributor.author | Chiu, Po Yuan | - |
dc.contributor.author | Chen, Yun | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Chen, Nien Jung | - |
dc.date.accessioned | 2020-11-17T14:55:48Z | - |
dc.date.available | 2020-11-17T14:55:48Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Journal of Biomedical Science, 2019, v. 26, n. 1, article no. 46 | - |
dc.identifier.issn | 1021-7770 | - |
dc.identifier.uri | http://hdl.handle.net/10722/292118 | - |
dc.description.abstract | Background: Triggering receptor expressed on myeloid cells-1 (TREM-1) is highly expressed on macrophages in inflamed intestines and reportedly promotes inflammatory bowel disease (IBD) by augmenting pro-inflammatory responses. To study the mechanism mediated by TREM-1 on macrophages, we generated an independent TREM-1 deficient mouse. Methods: Acute colitis was induced in C57BL/6 and TREM-1-deficient mice by the administration of dextran sodium sulfate (DSS). Colonic lamina propria immune cell composition and cytokines were analyzed. An innate lymphoid cell (ILC) co-culture experiment with macrophages was used to analyze IL-22 levels. Exogenous IL-22 and TREM-1-expressing macrophages were supplied to TREM-1-deficient mice for examining their effects on intestinal barrier integrity. Results: In inflamed colons, TREM-1 loss compromised the activation of ILC3 and their production of IL-22, which is required for intestinal barrier integrity. ILC3-mediated IL-22 production depends on IL-1β secreted by M1-polarized macrophages, and we found that TREM-1 deficiency results in a decreased number of IL-1β producing-M1 macrophages in colons exposed to DSS. Accordingly, DSS-mediated damage was ameliorated by supplying exogenous IL-22 and TREM-1-expressing macrophages to TREM-1-deficient mice. Conclusions: TREM-1 plays a crucial role in regulating IL-22 production by ILC3 through modulating M1-macrophage polarization during DSS-induced acute colitis. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Biomedical Science | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Triggering expressed on myeloid cells-1 | - |
dc.subject | Group 3 innate lymphoid cells | - |
dc.subject | Inflammatory macrophages | - |
dc.subject | IL-22 | - |
dc.subject | Colitis | - |
dc.title | TREM-1-dependent M1 macrophage polarization restores intestinal epithelium damaged by DSS-induced colitis by activating IL-22-producing innate lymphoid cells | - |
dc.type | Article | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1186/s12929-019-0539-4 | - |
dc.identifier.pmid | 31189465 | - |
dc.identifier.pmcid | PMC6560756 | - |
dc.identifier.scopus | eid_2-s2.0-85068165201 | - |
dc.identifier.volume | 26 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | article no. 46 | - |
dc.identifier.epage | article no. 46 | - |
dc.identifier.eissn | 1423-0127 | - |
dc.identifier.isi | WOS:000471272700001 | - |
dc.identifier.issnl | 1021-7770 | - |