Acute gastrointestinal syndrome is one of the components of acute radiation syndrome.
Experiments in our laboratory have shown that irradiation results in a dose-dependent
increase in plasma IL-1β levels. Secretion of IL-1β by activated macrophages depends on
interleukin-1β converting enzyme (ICE), termed caspase-1, that converts their precursors
to the mature and biologically active cytokines. NOD like receptor proteins are essential for
activation of caspase-1. IL-1β is a potent mediator of inflammation. At low concentrations,
IL-1β functions primarily to mediate local inflammation. However, if synthesized in larger
quantities, it can exert potentially lethal systemic effects. Although inflammatory response
is essential for wound healing, judicious use of anti-inflammatory agents are essential soon
after trauma to limit the extent of damage. We hypothesized that inhibiting NOD2 function
will help limit the initial radiation toxicity

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