RLRs as DExD/H-containing RNA helicases are expressed in the cytoplasm in a variety of cells, including immune and nonimmune cells. Unlike membranebond TLR3, TLR7 and TLR9, which are localized on the endosome and recognize viral double stranded RNA, singlestranded RNA and DNA, respectively, RLRs are cytoplasmic proteins that recognize viral RNA produced as a consequence of viral replication (20, 21) . RLRs consist of three family members: RIG-I, melanoma differentiation-associated gene 5 (MDA5) and laboratory of genetics and physiology 2 (LGP2) (21, 22) . Role of PRRs in mediating inflammation and organ injury. Infection causes PAMP release, but also causes tissue and cell damage and subsequent DAMP release. Similarly, injury caused by trauma or various other factors not only leads to DAMP release but also renders the patient more susceptible to infection and therefore PAMP release. In turn, the PAMPs and DAMPs act through PRRs, which include TLRs, NLRs and RLRs, to activate the innate immune system, yet they can also contribute to persistent and deleterious systemic inflammation and organ injury, including ALI. Structurally, RIG-I and MDA5 contain a DExD/H box RNA helicase domain and two caspase-recruiting domain (CARD)like domains required for eliciting downstream signaling pathways (23, 24) . The C-terminal region of RIG-I contains a repressor domain (RD), which inhibits downstream signaling. The MDA5 C-terminal region is similar to the RD of RIG-I; however, its function is not clear.