The recruitment of extra-intestinal cells to the injured mucosa promotes healing in radiation enteritis and chemical colitis in a mouse parabiosis model.
Animals
Antigens, Ly
/ metabolism
Bone Marrow Cells
/ physiology
Cell Movement
Colitis
/ chemically induced
Disease Models, Animal
Enteritis
/ therapy
Female
Humans
Intestinal Mucosa
/ physiology
Intestine, Small
/ physiology
Membrane Proteins
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Parabiosis
/ methods
Paracrine Communication
Radiation Injuries, Experimental
/ therapy
Receptors, CXCR4
/ metabolism
Trinitrobenzenesulfonic Acid
Wound Healing
Journal
Mucosal immunology
ISSN: 1935-3456
Titre abrégé: Mucosal Immunol
Pays: United States
ID NLM: 101299742
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
01
07
2018
accepted:
20
11
2018
revised:
05
11
2018
pubmed:
9
1
2019
medline:
25
6
2019
entrez:
9
1
2019
Statut:
ppublish
Résumé
Mucosal healing occurs through migration and proliferation of cells within injured epithelium, yet these processes may be inadequate for mucosal healing after significant injury where the mucosa is denuded. We hypothesize that extra-intestinal cells can contribute to mucosal healing after injury to the small and large intestine. We generated parabiotic pairs between wild-type and tdTomato mice, which were then subjected to radiation-induced enteritis and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. We now show that as compared with singleton mice, mice with a parabiotic partner were protected against intestinal damage as revealed by significantly reduced weight loss, reduced expression of pro-inflammatory cytokines, reduced enterocyte apoptosis, and improved crypt proliferation. Donor cells expressed CD45
Identifiants
pubmed: 30617302
doi: 10.1038/s41385-018-0123-3
pii: S1933-0219(22)00396-8
pmc: PMC6445662
mid: NIHMS1515486
doi:
Substances chimiques
Antigens, Ly
0
CXCR4 protein, mouse
0
Ly6a protein, mouse
0
Membrane Proteins
0
Receptors, CXCR4
0
Trinitrobenzenesulfonic Acid
8T3HQG2ZC4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
503-517Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK117186
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM078238
Pays : United States
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