ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023
A positive feedback cycle between the alarmin S100A8/A9 and NLRP3 inflammasome-GSDMD signalling reinforces the innate immune response in Candida albicans keratitis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 14 citations in OpenAlex.
- The Role of S100A8/A9 in Autoimmune Eye Diseases: From Pathogenesis to Targeted Therapy.Investigative ophthalmology & visual science · 2026Review
- Therapeutic Effects and Mechanisms of Sodium New Houttuyfonate in a Murine Model of Intra-AbdominalInternational journal of molecular sciences · 2026Article
- Cytokine signalling in vaginal epithelial cells: mechanistic insights into epithelial immunity and inflammatory milieu in vulvovaginal candidiasis.European cytokine network · 2026Review
- Identification of the Hub genes and inhibitors associated with hypertension in children with obesity using WGCNA.Frontiers in cardiovascular medicine · 2026Article
- Mechanisms and immune crosstalk of neutrophil extracellular traps in response to infection.mBio · 2025Review
- Single cell sequencing technology reveals the correlation between B lymphocytes and vascular inflammatory symptoms of Kawasaki disease.Translational pediatrics · 2025Article
- Article
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- The characteristics of microbiome in the upper respiratory tract of COVID-19 patients.BMC microbiology · 2024Article
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Authors and funding
8 authors at 5 institutions in 1 country.
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Abstract
objectiveFungal keratitis is a severe sight-threatening ocular infection, without effective treatment strategies available now. Calprotectin S100A8/A9 has recently attracted great attention as a critical alarmin modulating the innate immune response against microbial challenges. However, the unique role of S100A8/A9 in fungal keratitis is poorly understood.
methodsExperimental fungal keratitis was established in wild-type and gene knockout (TLR4
resultsHerein, we characterized the proteome of mouse corneas infected with Candida albicans and found that S100A8/A9 was robustly expressed at the early stage of the disease. S100A8/A9 significantly enhanced disease progression by promoting NLRP3 inflammasome activation and Caspase-1 maturation, accompanied by increased accumulation of macrophages in infected corneas. In response to Candida albicans infection, toll-like receptor 4 (TLR4) sensed extracellular S100A8/A9 and acted as a bridge between S100A8/A9 and NLRP3 inflammasome activation in mouse corneas. Furthermore, the deletion of TLR4 resulted in noticeable improvement in fungal keratitis. Remarkably, NLRP3/GSDMD-mediated macrophage pyroptosis in turn facilitates S100A8/A9 secretion during Candida albicans keratitis, thus forming a positive feedback cycle that amplifies the proinflammatory response in corneas.
conclusionsThe present study is the first to reveal the critical roles of the alarmin S100A8/A9 in the immunopathology of Candida albicans keratitis, highlighting a promising approach for therapeutic intervention in the future.
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