ArticleJournal of inflammation research2026
Inhibition of VNN1-Induced ROS-Dependent NETs Formation Alleviates Lung Injury and Systemic Inflammation in Sepsis Mice.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: Excessive neutrophil extracellular traps (NETs) formation worsens disease progression in sepsis. Vascular non-inflammatory molecule 1 (VNN1) is a glycosylphosphatidylinositol-anchored protein. The present study investigated the mechanism of the role of VNN1 in NETs formation and sepsis. Methods: Neutrophils from mouse bone marrow were isolated for experiments and mRNA sequencing. A cecum ligation and puncture-induced sepsis mouse model was established. Histopathological staining, real-time PCR, ELISA, flow cytometry and Western blot were used to detect phenotypic changes. Results: VNN1 induced ROS-dependent NETs formation in vitro. S100A9 increases VNN1 protein levels and promoted NET formation in a VNN1-dependent manner. VNN1 also induced the NETs formation in vivo. VNN1 inhibition might ameliorate lung injury in sepsis mice via the reduction of NETs formation. VNN1 inhibition alleviated systemic inflammation in sepsis mice. Meanwhile, VNN1 inhibition was associated with reduced neutrophil recruitment to inflammatory sites. RNA sequencing results showed that immune and inflammation-related pathways were significantly altered in sepsis mice treated with the VNN1 inhibitor. Conclusion: This study demonstrates that S100A9 increases VNN1 protein levels and induces VNN1-dependent NETs formation in vitro. Inhibition of VNN1 by PFI-653 blocks NADPH oxidase-derived ROS and thereby suppresses NETs formation. In vivo VNN1 inhibition alleviates lung injury and systemic inflammation in septic mice, potentially through the suppression of NET formation.
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