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Pathological Type-2 Immune Response, Enhanced Tumor Growth, and Glucose Intolerance in Retn/beta (RELM beta) Null Mice A Model of Intestinal Immune System Dysfunction in Disease Susceptibility

Artikel i vetenskaplig tidskrift
Författare Ingrid Wernstedt Asterholm
J. Y. Kim-Muller
J. M. Rutkowski
C. Crewe
C. Tao
P. E. Scherer
Publicerad i American Journal of Pathology
Volym 186
Nummer/häfte 9
Sidor 2404-2416
ISSN 0002-9440
Publiceringsår 2016
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor 2404-2416
Språk en
Länkar dx.doi.org/10.1016/j.ajpath.2016.04...
Ämnesord resistin-like-molecule, colorectal-cancer, adipose-tissue, colon-cancer, inflammatory responses, fvb mice, expression, colitis, promotes, carcinogenesis, Pathology
Ämneskategorier Klinisk medicin

Sammanfattning

Resistin, and its closely related homoldgs, the resistin-like molecules (RELMs) have been implicated in metabolic dysregulation, inflammation, and cancer. Specifically, REM beta expressed predominantly in the goblet cells in the colon, is released both apically and basolaterally, and is hence found in both the intestinal lumen in the mucosal layer as well as in the circulation. RELM beta has been linked to both the pathogenesis of colon cancer and type 2 diabetes. RELM beta plays a complex role in immune system regulation, and the impact of loss of function of RELM beta on colon cancer and metabolic regulation has not been fully elucidated. We therefore tested whether Retnl beta (mouse ortholog of human RETNL beta null mice have an enhanced or reduced susceptibility for colon cancer as well as metabolic dysfunction. We found that the lack of RELM beta Leads to increased colonic expression of T helper cell type-2 cytokines and IL-17, associated with a reduced ability to maintain intestinal homeostasis. This defect leads to an enhanced susceptibility to the development of inflammation, colorectal cancer, and glucose intolerance. In conclusion, the phenotype of the Retnl beta null mice unravels new aspects of inflammation-mediated diseases and strengthens the notion that a proper intestinal barrier function is essential to sustain a healthy phenotype.

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