Disruption of Pten speeds onset and increases severity of spontaneous colitis in Il10(-/-) mice.

ABSTRACT:

Background & aims

Early-onset ulcerative colitis, which is considered severe colonic inflammation that develops in infants and young children, can be caused by alterations in interleukin (IL)-10 signaling, although other factors are involved in its pathogenesis. We investigated whether loss of phosphatase and tensin homologue (PTEN), which regulates many important cell functions such as cell proliferation, cell survival, and Toll-like receptor (TLR) signaling pathways, contributes to the development of colitis in Il10(-/-) mice.

Methods

We generated Il10(-/-) mice (in C57BL/6 and C3H/HeJBir background strains) with disruption of Pten in the intestinal epithelium (Ints(ΔPten/ΔPten);Il10(-/-) mice) and Ints(ΔCont);Il10(-/-) (control) mice. Colon tissues were collected and hist

SUBMITTER: Im E 

PROVIDER: S-EPMC4143453 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature