Čes-slov Pediat 2026, 81(3):141-147 | DOI: 10.55095/CSPediatrie2026/027

From hyperinflammation to immunoparalysis: the role of neutrophil extracellular traps (NETs) in the pathogenesis of pediatric sepsis

Ľudmila Podracká¹, Alexandra Gaal Kovalčíková¹, Peter Celec², Michal Pastorek²

¹ Detská klinika, Lekárska fakulta, Univerzita Komenského a Národný ústav detských chorôb, Bratislava

² Ústav molekulárnej biomedicíny, Lekárska fakulta, Univerzita Komenského, Bratislava

Sepsis is a life-threatening clinical syndrome characterized by organ dysfunction resulting from a dysregulated host response to infection. Despite substantial advances in intensive care, sepsis remains a major cause of morbidity and mortality in the pediatric population. The

pathogenesis of sepsis involves a complex interaction between the pathogen and the host immune system, leading to activation of innate immunity, excessive production of inflammatory mediators, endothelial dysfunction, activation of coagulation pathways, and the development of microvascular injury. A hallmark of sepsis is the simultaneous presence of a hyperinflammatory response and sepsis-induced

immunosuppression, manifested by functional alterations of neutrophils, changes in granulopoiesis, lymphocyte apoptosis, and increased susceptibility to secondary infections. The resulting dysregulated immune response promotes progression to multiple organ dysfunction, which represents the principal determinant of patient prognosis. The aim of this review is to systematically summarize the key

pathophysiological mechanisms of sepsis, with a focus on innate immunity, the role of neutrophils and neutrophil extracellular traps, endothelial dysfunction, coagulopathy, and sepsis-induced immunosuppression.

Keywords: sepsis, pathogenesis, innate immunity, neutrophils, neutrophil extracellular traps, granulopoiesis, immunoparalysis, endothelium, multiple organ dysfunction

Accepted: April 8, 2026; Published: July 1, 2026  Show citation