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  1. Artikel: Intestinal Barrier Dysfunction and Microbial Translocation in Patients with First-Diagnosed Atrial Fibrillation.

    Blöbaum, Leon / Witkowski, Marco / Wegner, Max / Lammel, Stella / Schencke, Philipp-Alexander / Jakobs, Kai / Puccini, Marianna / Reißner, Daniela / Steffens, Daniel / Landmesser, Ulf / Rauch, Ursula / Friebel, Julian

    Biomedicines

    2023  Band 11, Heft 1

    Abstract: Background: According to the leaky gut concept, microbial products (e.g., lipopolysaccharide, LPS) enter the circulation and mediate pro-inflammatory immunological responses. Higher plasma LPS levels have been reported in patients with various ... ...

    Abstract Background: According to the leaky gut concept, microbial products (e.g., lipopolysaccharide, LPS) enter the circulation and mediate pro-inflammatory immunological responses. Higher plasma LPS levels have been reported in patients with various cardiovascular diseases, but not specifically during early atrial fibrillation (AF).
    Methods: We studied data and blood samples from patients presenting with first-diagnosed AF (FDAF) (
    Results: Circulating biomarkers that are suggestive of mucosal inflammation (zonulin, mucosal adhesion molecule MAdCAM-1) and intestinal epithelium damage (intestinal fatty acid binding protein, IFABP) were increased in the plasma of patients with FDAF when compared to patients with chronic cardiovascular diseases but without AF. Surrogate plasma markers of increased intestinal permeability (LPS, CD14, LPS-binding protein, gut-derived LPS-neutralising IgA antibodies, EndoCAbs) were detected during early AF. A reduced ratio of IgG/IgM EndoCAbs titres indicated chronic endotoxaemia. Collagen turnover biomarkers, which corresponded to the LPS values, suggested an association of gut-derived low-grade endotoxaemia with adverse structural remodelling. The LPS concentrations were higher in FDAF patients who experienced a major adverse cardiovascular event.
    Conclusions: Intestinal barrier dysfunction and microbial translocation accompany FDAF. Improving gut permeability and low-grade endotoxaemia might be a potential therapeutic approach to reducing the disease progression and cardiovascular complications in FDAF.
    Sprache Englisch
    Erscheinungsdatum 2023-01-10
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11010176
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Cytotoxic CD8

    Friebel, Julian / Witkowski, Marco / Wegner, Max / Blöbaum, Leon / Lammel, Stella / Schencke, Philipp-Alexander / Jakobs, Kai / Puccini, Marianna / Reißner, Daniela / Steffens, Daniel / Moos, Verena / Schutheiss, Heinz-Peter / Landmesser, Ulf / Rauch, Ursula

    Cells

    2022  Band 12, Heft 1

    Abstract: Background: Atrial myopathy and atrial fibrillation (AF) accompany thrombo-inflammation. This facilitates disease progression and promotes major adverse cardiovascular events (MACEs). Thrombin receptor (protease-activated receptor 1, PAR1) signalling is ...

    Abstract Background: Atrial myopathy and atrial fibrillation (AF) accompany thrombo-inflammation. This facilitates disease progression and promotes major adverse cardiovascular events (MACEs). Thrombin receptor (protease-activated receptor 1, PAR1) signalling is central in mediating thrombo-inflammation. We hypothesised that PAR1 signalling links coagulation and inflammation through cytotoxic CD8
    Methods: A total of 210 patients were studied. We included data and blood samples from patients presenting with FDAF (
    Results: During early AF, a pro-inflammatory and cytotoxic subset of T lymphocytes (CD8
    Conclusions: In patients with FDAF, the TF-factor Xa-factor IIa-axis contributes to thrombo-inflammation via PAR1 in CD8
    Mesh-Begriff(e) Humans ; Atrial Fibrillation ; Receptor, PAR-1 ; CD8-Positive T-Lymphocytes ; Inflammation/complications ; Disease Progression
    Chemische Substanzen Receptor, PAR-1
    Sprache Englisch
    Erscheinungsdatum 2022-12-29
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12010141
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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