Human β2-glycoprotein I attenuates mouse intestinal ischemia/reperfusion induced injury and inflammation.

ABSTRACT: Intestinal ischemia-reperfusion (IR)-induced injury results from a complex cascade of inflammatory components. In the mouse model of intestinal IR, the serum protein, β2-glycoprotein I (β2-GPI) binds to the cell surface early in the cascade. The bound β2-GPI undergoes a conformational change which exposes a neoantigen recognized by naturally occurring antibodies and initiates the complement cascade. We hypothesized that providing additional antigen with exogenous β2-GPI would alter IR-induced tissue injury. Administration of human but not mouse β2-GPI attenuated IR-induced tissue damage and prostaglandin E(2) production indicating a physiological difference between β2-GPI isolated from the two species. To investigate whether structural features were responsible for this physiological diffe

SUBMITTER: Tomasi M 

PROVIDER: S-EPMC3565431 | biostudies-literature | 2012 Oct

REPOSITORIES: biostudies-literature