A Pathophysiological Insight into Sepsis and Its Correlation with Postmortem Diagnosis

Figure 1

Schematic of events associated with major mediators of cytokine cascade on initiation of sepsis. The release of a large amount of pathogen and damage associated molecular patterns (PAMPs and DAMPs) from invading microorganisms and/or damaged host tissue, respectively, results in the overstimulation of pattern-recognition receptors (PRRs) of immune cells. This process activates an inflammatory cascade in which large amounts of cytokines are released into the body. Macrophages and endothelial cells are then hyperactivated by the unusually large quantity of circulating cytokines. The activation of macrophages and endothelial cells results in the release of more cytokines, exacerbating the inflammatory response. The profound proinflammatory response is counteracted by certain anti-inflammatory cytokines, including IL-10, transforming growth factor-β (TGF-β), and IL-4, which attempt to restore immunological equilibrium.