NDLI: Efficient colonic mucosal wound repair requires Trem2 signaling

Content Provider	PubMed Central
Author	Seno, Hiroshi Miyoshi, Hiroyuki Brown, Sarah L. Geske, Michael J. Colonna, Marco Stappenbeck, Thaddeus S.
Abstract	The colonic epithelial lining undergoes constant replacement, driven by epithelial stem cells in crypts of Lieberkühn. Stem cells lost because of damage or disease can be replaced by adjacent crypts that undergo fission. The close proximity of an extraordinary number of luminal microbes creates a challenge for this repair process; infection must be prevented while immune system activation and epithelial stem cell genetic damage must be minimized. To understand the factors that modulate crypt/stem cell replacement in the mouse colon, we developed an in vivo acute injury system analogous to punch biopsy of the skin. In contrast to epidermal stem cells, colonic epithelial progenitors did not migrate over the wound bed. Instead, their proliferative expansion was confined to crypts adjacent to wound beds and was delayed to the latter phase of healing. This increased epithelial proliferation was coincident with the infiltration of Trem2 expressing macrophages and increased expression of IL-4 and IL-13 in the wound bed. Interestingly, Trem2 −/− mice displayed slow and incomplete wound healing of colonic mucosal injuries. We found the latter phase of healing in Trem2 −/− mice showed a diminished burst of epithelial proliferation, increased expression of IFN-γ and TNF-α, diminished expression of IL-4 and IL-13, and increased markers of classical macrophage activation. Ablation of these cytokines in injured WT and Trem2 −/− mice demonstrated that their expression ultimately determined the rate and nature of wound healing. These studies show that Trem2 signaling is an important pathway to promote healing of wounds in the colon where stem cell replacement is necessary.
Related Links	http://dx.doi.org/10.1073/pnas.0803343106
Ending Page	261
Page Count	6
Starting Page	256
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	1
Volume Number	106
Language	English
Publisher	National Academy of Sciences
Publisher Date	2009-01-06
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Redox signaling between DNA repair proteins for efficient lesion detection

Highly efficient differentiation of hESCs to functional hepatic endoderm requires ActivinA and Wnt3a signaling

The Toll/NF-κB signaling pathway is required for epidermal wound repair in Drosophila

Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair

Mucosal adjuvant activity of cholera toxin requires Th17 cells and protects against inhalation anthrax

Trk retrograde signaling requires persistent, Pincher-directed endosomes

PI3K/Akt signaling requires spatial compartmentalization in plasma membrane microdomains

Correct biological timing in Arabidopsis requires multiple light-signaling pathways

The wound repair response controls outcome to cutaneous leishmaniasis

Efficient colonic mucosal wound repair requires Trem2 signaling

Similar Documents

Redox signaling between DNA repair proteins for efficient lesion detection

Highly efficient differentiation of hESCs to functional hepatic endoderm requires ActivinA and Wnt3a signaling

The Toll/NF-κB signaling pathway is required for epidermal wound repair in Drosophila

Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair

Mucosal adjuvant activity of cholera toxin requires Th17 cells and protects against inhalation anthrax

Trk retrograde signaling requires persistent, Pincher-directed endosomes

PI3K/Akt signaling requires spatial compartmentalization in plasma membrane microdomains

Correct biological timing in Arabidopsis requires multiple light-signaling pathways

The wound repair response controls outcome to cutaneous leishmaniasis

Efficient colonic mucosal wound repair requires Trem2 signaling