ArticleNature communications2022
Differential dysregulation of granule subsets in WASH-deficient neutrophil leukocytes resulting in inflammation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Munc13-4-STX7 inhibitors impair endosomal TLR activation and systemic inflammation.Nature chemical biology · 2026Article
- Mitochondrial activity promotes neutrophil degranulation and endothelial dysfunction in systemic infections.EMBO molecular medicine · 2026Article
- WASH regulates B cell signaling, metabolism and function through STAT1.Cell death and differentiation · 2026Article
- Inhaled bovine lactoferrin modulates the p47phox-MPO-NETosis axis in acute lung injury: implications for bioengineered nanomedicine in respiratory infections.Frontiers in immunology · 2026Article
- Harnessing neutrophils for tissue repair and regeneration: mechanisms, biomaterial engineering strategies and translational potential.Regenerative biomaterials · 2026Review
- Nexinhib20 inhibits JFC1-mediated mobilization of a subset of CD11b/CD18+ vesicles decreasing integrin avidity, but does not inhibit Rac1.Journal of leukocyte biology · 2025Article
- Article
- Obtaining super-resolved images at the mesoscale through super-resolution radial fluctuations.Journal of biomedical optics · 2024Article
- Defective endomembrane dynamics in Rab27a deficiency impairs nucleic acid sensing and cytokine secretion in immune cells.Cell reports · 2024Article
- Reconstitution of Rab11-FIP4 Expression Rescues Cellular Homeostasis in Cystinosis.Molecular and cellular biology · 2024Article
- Platelet-Rich Plasma in Dermatology: New Insights on the Cellular Mechanism of Skin Repair and Regeneration.Life (Basel, Switzerland) · 2023Review
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Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Dysregulated secretion in neutrophil leukocytes associates with human inflammatory disease. The exocytosis response to triggering stimuli is sequential; gelatinase granules modulate the initiation of the innate immune response, followed by the release of pro-inflammatory azurophilic granules, requiring stronger stimulation. Exocytosis requires actin depolymerization which is actively counteracted under non-stimulatory conditions. Here we show that the actin nucleator, WASH, is necessary to maintain azurophilic granules in their refractory state by granule actin entrapment and interference with the Rab27a-JFC1 exocytic machinery. On the contrary, gelatinase granules of WASH-deficient neutrophil leukocytes are characterized by decreased Rac1, shortened granule-associated actin comets and impaired exocytosis. Rac1 activation restores exocytosis of these granules. In vivo, WASH deficiency induces exacerbated azurophilic granule exocytosis, inflammation, and decreased survival. WASH deficiency thus differentially impacts neutrophil granule subtypes, impairing exocytosis of granules that mediate the initiation of the neutrophil innate response while exacerbating pro-inflammatory granule secretion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.