These pharmacological interventions also attenuated the elevated protein expression of toll-like receptor 4 (TLR4) and monocyte chemoattractant protein-1 (MCP1) in the brainstem nucleus tractus solitarius (NTS) of morphine-treated CLP rats.<h4>Conclusion</h4>Overall, morphine augments the sepsis-induced depression of reflex cardiovagal activity through an opioid receptor sensitive mechanism that engages brainstem inflammatory and chemotactic circuits related to PI3K/MAPK/NADPHox/ROCK signaling. This evidence concerns the gene TLR4 and Sepsis.