ArticleJournal of inflammation research2026
Injury-Induced Epithelial Spp1 Engages Cd44 to Promote Neutrophil Recruitment and Exacerbate Acute Kidney Injury.
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. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- A cross-model single-cell atlas reveals conserved involvement of osteopontin in polycystic kidney disease.JCI insight · 2026Article
- Long-term polystyrene nanoplastics exposure aggravates retinal inflammation and photoreceptor degeneration through microglial SPP1 signaling and neutrophil extracellular traps formation.Journal of translational medicine · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Background: Acute kidney injury (AKI) severely impairs renal function. In early AKI, tubular cells release damage-associated molecular patterns (DAMPs) that induce neutrophil recruitment. Infiltrating neutrophils can exacerbate kidney injury through degranulation or formation of neutrophil extracellular traps (NETs), but the specific DAMPs mediating early neutrophil chemotaxis remain unclear. Methods: We integrated single-cell and spatial transcriptomic data from early AKI kidneys to identify signaling pathways underlying crosstalk between injured tubular cells and neutrophils. A murine unilateral ischemia-reperfusion injury (uIRI) model was then established, with intraperitoneal administration of the anti-inflammatory drug mesalazine (5-aminosalicylic acid, 5-ASA) during the perioperative period, followed by assessment of renal histopathology and function. In vitro, polymorphonuclear neutrophils (PMNs) were isolated from mouse peripheral blood and co-cultured with renal tubular cells in a Transwell migration system under hypoxia/reoxygenation (H/R), with 5-ASA treatment or Spp1 knockdown to evaluate effects on PMN migration. Results: Integrated single-cell and spatial transcriptomic analyses revealed that injured tubular cells upregulate Spp1, which interacts with Cd44 on neutrophils. In vivo and in vitro, injured tubular cells released Spp1 in a paracrine manner, enhancing Cd44 Conclusion: This study provides the first evidence that tubular cell-derived Spp1 functions as a key DAMP mediating the early recruitment of Cd44
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