Abstract
According to the current understanding of the pathophysiology of sepsis, key host dysregulated responses leading to organ failure are mediated by innate immunity, through interactions between pathogen-associated molecular patterns (PAMPs) and damaged-associated molecular patterns (DAMPs) binding to four types of pattern recognition receptors (PRRs). PRRs activation triggers the protein kinase cascade, initiating the cellular response seen during sepsis. Pancreatic stone protein (PSP), a C-type lectin protein, is a well-defined biomarker of sepsis. Studies have shown that stressed and immune-activated pancreatic β-cells secrete PSP. Animal studies have shown that PSP injection aggravates sepsis, and that the disease severity score and mortality were directly correlated with the doses of PSP injected. In humans, studies have shown that PSP activates polymorphonuclear neutrophils (PMNs) and aggravates multiple organ dysfunction syndrome. Clinical studies have shown that PSP levels are correlated with disease severity, vasopressor support, progression to organ failure, mechanical ventilation, renal replacement therapy, length of stay, and mortality. As PSP is a C-type lectin protein, it may have a role in activating innate immunity through the C-type lectin receptors (CLRs), which is one of the four PRRs. Herein, we review the literature on PSP and its possible role in the pathophysiology of sepsis, and we discuss its potential therapeutic role.