A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Oral microbiome dysbiosis in cryptogenic ischemic stroke patients with high-risk patent foramen ovale
Tekijät: Manzoor, Muhammed; Leskelä, Jaakko; Pietiäinen, Milla; Martinez-Majander, Nicolas; Könönen, Eija; Sinisalo, Juha; Putaala, Jukka; Pussinen, Pirkko J.; Paju, Susanna
Kustantaja: Springer Science and Business Media LLC
Kustannuspaikka: BERLIN
Julkaisuvuosi: 2025
Journal: Scientific Reports
Tietokannassa oleva lehden nimi: Scientific Reports
Lehden akronyymi: SCI REP-UK
Artikkelin numero: 11535
Vuosikerta: 15
Numero: 1
Sivujen määrä: 14
ISSN: 2045-2322
eISSN: 2045-2322
DOI: https://doi.org/10.1038/s41598-025-95728-x
Verkko-osoite: https://doi.org/10.1038/s41598-025-95728-x
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/491821520
Patent foramen ovale (PFO) is the most common congenital heart abnormality of foetal origin and has been associated with cryptogenic ischemic stroke (CIS) through several mechanisms, with most theories supporting paradoxical embolism. Other possible but unknown contributing factors, such as the role of the microbiome in PFO-associated strokes, remain unclear. We analysed saliva metagenomes to study the differences in the oral microbiome between young-onset CIS patients with clinically relevant high-risk PFO (n = 52) and those without PFO (n = 52). Age- and sex-matched stroke-free controls (n = 16) with high-risk PFO were included for the comparison. Beta diversity was significantly different between patients and controls with high-risk PFO, but not between patients with and without high-risk PFO. The phylum Ascomycota and class Saccharomycetes were significantly more abundant in patients with high-risk PFO than in those without high-risk PFO. Additionally, the abundance of Lactococcus, including Lactococcus raffinolactis and L. cremoris, was higher in controls with high-risk PFO than in patients with high-risk PFO. These findings highlight that oral dysbiosis and high-risk PFO may form a critical but under-recognized combination in the aetiology of CIS. Future research should focus on elucidating the precise mechanisms of these interactions and developing targeted interventions.
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This work was supported by the Academy of Finland grants (316777 and 355532 for SP; 340750 for PJP; 286246, 318075, 322656 for JP), the Finnish Dental Society Apollonia (for PJP), and the Sigrid Jusélius Foundation (for PJP), the Finnish Medical Foundation (for JP), the Helsinki and Uusimaa Hospital District (TYH2014407, TYH2018318 for JP), and the Minerva Foundation Selma and Maja-Lisa Selander’s Fund (for MM). Open access funded by Helsinki University Library. The funders had no role in the design or execution of the study; the collection, management, analysis, or interpretation of data; the preparation, review, or approval of the manuscript; or the decision to submit the manuscript for publication.
