Serum CCL1 discriminates infectious and sterile systemic inflammation in sepsis and acute pancreatitis.

Differentiating between infectious and non-infectious etiologies in systemic inflammatory disorders may be challenging due to overlapping clinical presentations and the lack of reliable discriminating biomarkers. Regulatory T-cells (Tregs) modulate immune responses. Their functionality is governed by specific chemokines, including CCL1 and CCL22. We investigated whether these Treg-attracting chemokines are differentially regulated in infectious versus sterile inflammation. This prospective, single-center biomarker study enrolled patients with sepsis, acute pancreatitis, and hospitalized controls without infectious diseases. Serum samples were collected on days 1, 3, 5, and 7, measuring CRP, IL-6, PCT, CCL1, and CCL22. Between March 2019 and October 2022, 159 patients were enrolled, comprising 45 patients suffering from acute pancreatitis, 15 patients with confirmed sepsis as well as 99 hospitalized controls. Established inflammatory parameters CRP, IL-6 and PCT showed typical kinetics. Decreased CCL1 levels, but not CCL22, distinguished acute pancreatitis from sepsis at all time points. Additionally, CCL1 levels inversely correlated with organ failure severity in sepsis patients. CCL1 shows potential to serve as a biomarker to differentiate sterile and non-sterile inflammation in sepsis and acute pancreatitis. This may support clinical decision-making and allow a more precise use of antibiotics in these patient cohorts.