ArticleExperimental dermatology2021
Evaluation of neutrophil extracellular trap deregulated formation in pyoderma gangrenosum.
Article in Experimental dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Role of T Helper 2 Signaling in the Regulation of Neutrophil Extracellular Trap Formation in Pyoderma Gangrenosum.The Journal of investigative dermatology · 2026Article
- Gasdermin D-dependent neutrophil extracellular traps exacerbate cytokine storm contributing to pyoderma gangrenosum pathogenesis.iScience · 2025Article
- Review
- Neutrophil extracellular traps and neutrophilic dermatosis: an update review.Cell death discovery · 2024Review
- NETosis Is Induced by Complement Component 5a: Implications in the Pathogenesis of Pyoderma Gangrenosum.The Journal of investigative dermatology · 2024Article
- Neutrophil Extracellular Traps in Skin Diseases.Biomedicines · 2021Review
- Evaluation of neutrophil extracellular trap deregulated formation in pyoderma gangrenosum.Experimental dermatology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pyoderma gangrenosum (PG) is a neutrophilic dermatose (ND) characterized by a dense neutrophilic infiltrate in the affected tissue. Neutrophil extracellular traps (NETs) are web-like structures released by neutrophils and composed of cytosolic and granule proteins assembled on a scaffold of decondensed chromatin. Very little is known about the role of NETosis in PG. Here, we assessed the possible implication of NETosis in the pathogenesis of PG by investigating the NETosis in the ulcers of 26 PG patients. We demonstrated that neutrophils in the PG skin lesions undergo an aberrant level of NETosis in 100% of the analysed cases (N = 26). All control and abscess biopsies were instead negative for the NETosis. In addition, neutrophils from peripheral blood of PG patients showed a significantly higher rate of spontaneous, but not induced, NETosis. Overall, this study suggests that the NETosis may contribute to systemic inflammation and tissue destruction in PG, thus representing a possible novel therapeutic target.
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