In the current study, we add the possibility that extrapulmonary endotoxemia secondary to enhanced gastrointestinal permeability with Poly(I:C)-MTV underlies this synergistic effect and reveal a role for intracellular LPS mediated caspase-11 activation, a non-canonical inflammasome pathway and interactions of caspase-11 and caspase-1 in lung injury. The gene discussed is CASP1; the disease is serum lipopolysaccharide activity.