3.1 Imbalance of inflammatory response
When pathogenic microorganisms and virulence factors invade the body, the body activates the innate immune system through a series of inflammatory reactions to resist pathogen infection. However, when the inflammatory reaction is over-activated, it will cause organ dysfunction and further aggravate the injury. Inflammatory cytokines play an important role in the progression of sepsis and are involved in multiple organ injury in sepsis. At present, most scholars believe that the pro-inflammatory factor TNF- α is not only the ”core factor” causing dysfunction and injury of many important organs, but also the initiating factor, and is closely related to IL-1β Play a synergistic effect[24]. IL- 1β As another key inflammatory factor, studies have found that inhibition of IL-1β Expression can reduce hemodynamic and metabolic disorders in severe sepsis[25]. In addition, IL-1β Can promote monocyte chemoattractant protein-1, I-κBα. The synthesis of multiple inflammatory genes, such as MKP-1 and other interleukin-like cytokines, further promotes the spread of inflammatory reaction and causes sepsis-related organ dysfunction[26]. During lipopolysaccharide LPS-induced sepsis, HMGB1 can cause multiple tissue and organ damage through different mechanisms, such as lung, kidney, liver, cardiovascular, and nervous systems[27]. Fu[28] and other researchers believe that HMGB1 is over-regulated in sepsis, and experiments have confirmed that HMGB1 has a protective effect on septic liver injury by targeting HMGB1. When cells are stimulated by pathogenic microorganisms and bacterial products, nuclear factor κ B (NF- κ B) Nuclear translocation and its promoter will be activated, leading to the release of pro-inflammatory factors, including TNF- α、IL-1β. At the same time, these inflammatory factors will further positively feedback and activate NF- κ B. Lead to the imbalance of inflammatory response and then aggravate sepsis.