Innate immunity against bacterial infection following hyperoxia exposure is impaired in NRF2-deficient mice.

ABSTRACT: Oxygen supplementation is used as therapy to support critically ill patients with severe respiratory impairment. Although hyperoxia has been shown to enhance the lung susceptibility to subsequent bacterial infection, the mechanisms underlying enhanced susceptibility remain enigmatic. We have reported that disruption of NF-E2-related factor 2 (Nrf2), a master transcription regulator of various stress response pathways, enhances susceptibility to hyperoxia-induced acute lung injury in mice, and have also demonstrated an association between a polymorphism in the NRF2 promoter and increased susceptibility to acute lung injury. In this study, we show that Nrf2-deficient (Nrf2(-/-)) but not wild-type (Nrf2(+/+)) mice exposed to sublethal hyperoxia succumbed to death during recovery after Pseudom

SUBMITTER: Reddy NM 

PROVIDER: S-EPMC2820249 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature