{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T18:00:46Z","timestamp":1793037646215,"version":"4.5.0"},"reference-count":93,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T00:00:00Z","timestamp":1765411200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Emerging evidence underscores the critical role of microbiota dysbiosis in autoimmune pathogenesis, yet direct links between specific microbial species and disease mechanisms remain poorly defined. Our prior work identified\n                    <jats:italic>Kazachstania pintolopesii<\/jats:italic>\n                    , a gut-dwelling fungus isolated from spontaneous ankylosing spondylitis (AS)-prone monkeys, as a potent inducer of PANoptosome assembly. However, the multicellular and molecular mechanisms underlying its pathogenicity remained elusive. Here, we elucidate how lysates of\n                    <jats:italic>K. pintolopesii<\/jats:italic>\n                    (LKP) disrupt immune homeostasis through immune-endothelial-fibroblast crosstalk, metabolic reprogramming, and dysregulated cytokine networks in genetically susceptible hosts. Using single-nucleus RNA sequencing and functional assays, we demonstrate that LKP triggers robust inflammatory arthritis and tissue fibrosis in\n                    <jats:italic>BALB\/c ZAP70W163C<\/jats:italic>\n                    mutant mice. Results showed that LKP injection induces severe joint destruction, spinal deformities, and upregulation of pro-inflammatory cytokines (IL-1\u03b2, IL-6, NF-\u03baB) in joint tissues; immune-endothelial-fibroblast networks are dysregulated, with T cells promoting osteoclastogenesis via ligand-receptor interactions (e.g.,\n                    <jats:italic>Sema4d-Plxnb1<\/jats:italic>\n                    ) and endothelial cells exhibiting impaired migratory capacity and glycolytic reprogramming; fibroblast-like synoviocytes (FLS) undergo abnormal proliferation, with subpopulations (e.g., Fib_\n                    <jats:italic>Cmss1<\/jats:italic>\n                    , Fib_\n                    <jats:italic>Tnc<\/jats:italic>\n                    ) driving extracellular matrix remodeling through TGF-\u03b2\/PI3K-Akt signaling; and distinct macrophage subtypes (e.g., Mac_\n                    <jats:italic>Adam8<\/jats:italic>\n                    , Mac_\n                    <jats:italic>mt-Col<\/jats:italic>\n                    ) exhibit ferroptosis and PI3K-Akt activation, contributing to osteoclastogenesis and cartilage degradation. Mechanistically, LKP disrupts mitochondrial function, enhances IL-17\/TNF-\u03b1 signaling, and induces pan-inflammatory responses in genetically predisposed hosts. Therapeutic targeting of these pathways (e.g., IL-17\/IL-6 inhibitors, metabolic modulators) may disrupt the pathogenic cascade. Our findings establish\n                    <jats:italic>K. pintolopesii<\/jats:italic>\n                    as a keystone pathobiont in autoimmune arthritis and fibrosis, offering actionable insights for precision medicine.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2025.1738184","type":"journal-article","created":{"date-parts":[[2025,12,11]],"date-time":"2025-12-11T05:19:56Z","timestamp":1765430396000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Kazachstania pintolopesii triggers an immune-endothelial-fibroblast cascade and drives inflammatory arthritis and tissue fibrosis in genetically susceptible hosts"],"prefix":"10.3389","volume":"15","author":[{"given":"Haiting","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Duanling","family":"Tan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chulan","family":"Lin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanqing","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diling","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,12,11]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"810","DOI":"10.1093\/mmy\/myz126","article-title":"Encephalitozoon intestinalis: A new target for auranofin in a mice model","volume":"58","author":"Abou-El-Naga","year":"2020","journal-title":"Med. 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