title: The ANXA1 released from intestinal epithelial cells alleviate DSS-induced colitis by improving NKG2A expression of Natural Killer cells.
abstract: Inflammatory bowel disease (IBD) arises when intestinal immune homeostasis is broken, the maintenance of such homeostasis is principally controlled by cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells (IECs). IECs can prevent the contact between luminal bacteria with immune cells through the formation of a physical barrier and the expression of antimicrobial peptides to maintain intestinal immune homeostasis. During Colitis the IECs can express increased ANXA1, which is important for regeneration of intestinal mucosa and function as a potent anti-inflammatory protein. Natural Killer (NK) cells can also suppress the progression of colitis. It is uncertain about the effect of the cross-talk between injured IECs and recruited NK cells during colitis. In this study, the expression of ANXA1 in IECS from DSS treated mice was increased, and more NK cells were recruited to intestinal mucosa. In addition, the expression of NKG2A was upregulated when co-cultured with NK cells. The results further proved that overexpression of NKG2A in NK cells was important for inhibiting the recruitment and activity of neutrophils to alleviate DSS-induced colitis. Here, we provide a new anti-inflammation mechanism about ANXA1 secreted from injured IECs, where ANXA1 can stimulate the expression of NKG2A in NK cells that affect the recruitment and activity of neutrophils necessary for pathology of colitis.
authors.affiliation: Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, 430022, PR China.
authors.forename: Z
authors.initials: Z
authors.lastname: Zou
authors.affiliation: Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, 430022, PR China.
authors.forename: D
authors.initials: D
authors.lastname: Zuo
authors.affiliation: Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, 430022, PR China.
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, 430022, PR China. Electronic address: fanheng009@aliyun.com.
authors.forename: H
authors.initials: H
authors.lastname: Fan
mesh_terms: D000818:Animals; D017305:Annexin A1 / Q000096:biosynthesis*; D002450:Cell Communication; D002478:Cells, Cultured; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D016264:Dextran Sulfate; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D007413:Intestinal Mucosa / Q000378:metabolism* / Q000473:pathology; D007694:Killer Cells, Natural / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000378:metabolism*
chemical_list: D017305:Annexin A1; D055654:NK Cell Lectin-Like Receptor Subfamily C; C573274:annexin A1, mouse; D016264:Dextran Sulfate
keywords: ANXA1; Colitis; Intestinal epithelial cells; NKG2A; Natural killer cells