NET degradation attenuates ricin-induced acute lung injury and protects mice from ARDS.

ABSTRACT:

Background

Neutrophils are critical first responders of the innate immune system, rapidly recruited to sites of infection or sterile injury. Upon activation by pathogen- or damage-associated molecular patterns, neutrophils initiate antimicrobial responses, including cytokine release, phagocytosis, and the formation of neutrophil extracellular traps (NETs). While NETosis plays a protective role, excessive NET formation can exacerbate inflammation and tissue damage. Pulmonary exposure to ricin, a potent toxin derived from Ricinus communis, results in acute lung injury characterized by neutrophil infiltration, cytokine production, vascular leakage, and pulmonary edema. This study investigated the contribution of NETosis to ricin-induced lung pathology and explored the therapeutic pote

SUBMITTER: Sapoznikov A 

PROVIDER: S-EPMC12481763 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature