BPOZ-2-deficient mice exhibit aggravated inflammation-associated tissue damage after acute dextran sodium sulfate or diethylnitrosamine exposure.

An excessive inflammatory response plays an important role in pathological tissue damage associated with pathogen infection and tumorigenesis. Blood POZ-containing gene type 2 (BPOZ-2), an adaptor protein for the E3 ubiquitin ligase scaffold protein CUL3, is a negative regulator of the inflammatory response. In this study, we investigated the pathophysiological functions of BPOZ-2 in dextran sodium sulfate (DSS)-induced colon injury and diethylnitrosamine (DEN)-induced liver damage. Our results indicated that BPOZ-2 deficiency increased IL-1β induction after DSS and DEN treatment. In addition, BPOZ-2-deficient mice were more susceptible to DSS-induced colitis. Notably, BPOZ-2 deficiency aggravated DEN-induced acute liver injury. These results revealed that BPOZ-2 protected against pathological tissue damage with a dysregulated inflammatory response. • BPOZ-2-deficient mice are more susceptible to DSS-induced colitis and aggravates DEN-induced acute liver injury. • BPOZ-2 deficiency increases the inflammatory response in response to DSS and DEN treatment. • BPOZ-2 is a negative regulator of the inflammatory response. [ABSTRACT FROM AUTHOR]