Mitochondrial superoxide increase is essential for Caenorhabditis elegans against Enterococcus faecalis infection

Abstract

Enterococcus faecalis infection can cause serious diseases including cancer development.
Recently it has been reported that mitochondrial reactive oxygen species (mROS) are required for host immune defenses against bacteria and many mutations in mitochondrial electron transport chain (mETC) genes have an effect on mROS production. To identify the exact role of mROS during E. faecalis infection, we thus decide to knockdown the expression of mev-1 and isp-1 in Caenorhabditis elegans using RNAi. The knockdown of mev-1 and isp-1 causes increased susceptibility and increased resistance to E. faecalis infection, respectively. The mev-1(RNAi) can also down-regulate antimicrobial genes (C17H12.8, mtl-1 and bli-3), whereas these antimicrobial genes are up-regulated in isp-1(RNAi) animals after bacterial infection. Further, significant increase of mitochondrial superoxide and mitochondrial sod expressions have been observed in isp-1(RNAi) animals. Conversely, the mev-1(RNAi) worms show a decrease of mitochondrial superoxide and mitochondrial sod expressions. Prooxidant paraquat, which is a mitochondrial superoxide generator, can increase survival rate of mev-1(RNAi) animals after E. faecalis infection. All together, the enhancement of mitochondrial superoxide contributes to anti-bacterial immunity and a better knowledge of them should open new avenues for preventive strategies against bacterial infection and also limiting the development of infection-associated cancer.