NLRC4 gene silencing-dependent blockade of NOD-like receptor pathway inhibits inflammation, reduces proliferation and increases apoptosis of dendritic cells in mice with septic shock

Septic shock is one of the most significant health concerns across world, involving hypo-perfusion and defects in tissue energy. The current study investigates role NLR family CARD domain containing protein 4 (NLRC4) septic shock-induced inflammatory reactions, lung injuries, dendritic cell (DC) apoptosis. mice models were established by modified cecal ligation puncture injected with retroviral vector expressing siRNA-NLRC4. DCs then isolated transfected degree injury, cycle distribution, apoptosis viability assessed. NLRC4 was found to be expressed at high levels shock. silencing inhibited activation NOD-like receptor (NLR) pathway as evidenced decreased NOD1, NOD2, RIP2, NF-κB. In addition, reduced reaction attributed IL-1β, TNF-α IL-6. Suppressed promoted induction DC surface markers (CD80, CD86, MHC II), along alleviated injury. conclusion, ameliorates injury inflammation induced negatively regulating pathway.