SHIP1 DELETION ENHANCES ROS PRODUCTION AND DECREASES SURVIVAL OF THE S. AUREUS INFECTED MICE

Reactive oxygen species (ROS) production by neutrophils is essential for host innate immune defense. However, although ROS production is advantageous for killing various infectious organisms, excessive ROS can cause tissue damage. Thus, ROS production by neutrophils must be tightly controlled. In this study, we investigated a role for SH2 domain-containing inositol- 5-phosphatase 1 (SHIP1), a PtdIns(3,4,5)P3 phosphatase, in ROS production by neutrophils using ship1−/− mice. SHIP1 deletion enhanced ROS production as well as the bacterial killing capability of neutrophils. However, the ship1−/− mice showed decreases survival of the mice infected with Staphylococcus aureus (S. aureus). Our results suggest that SHIP1 controls appropriate host defenses against S. aureus infections in mice