You will find additional studies showing that infections may trigger APS in other rheumatic diseases, suggesting a microbial origin for both pathogenic and non-pathogenic aCl (Amital et al

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You will find additional studies showing that infections may trigger APS in other rheumatic diseases, suggesting a microbial origin for both pathogenic and non-pathogenic aCl (Amital et al., 2008). induce mutually cross-reactive Fevipiprant antibodies with the potential to be pathogenic (Wang et al., 2008). You will find additional studies showing that infections may trigger APS in other rheumatic diseases, suggesting a microbial origin for both pathogenic and non-pathogenic aCl (Amital et al., 2008). In periodontitis, this type of antibacterial immune response could be in part responsible for associations of periodontal infections with adverse cardiovascular and pregnancy outcomes in some patients, or they merely may be markers of events that co-occur with these conditions. We consider it unlikely that aCl in periodontitis patients are true autoantibodies in that the presence of autoimmune disease was an exclusion criterion for this study. In summary, IgG from patients with periodontitis who also have elevated serum concentrations of aCl stimulates increased production of the key cytokine MCP-1 from HUVEC cultures. Since periodontitis patients with no evidence of systemic disease demonstrate a significantly higher prevalence of elevated serum levels of aCl compared to periodontally Fevipiprant healthy Fevipiprant subjects, and since these potentially pathogenic antibodies may be induced by a variety of periodontal pathogens, it is proposed that molecular mimicry with the production of aCl could be one pathogenic link between periodontal contamination and systemic disease. ? Clinical Relevance Scientific Rationale for the Study Anticardiolipin antibodies, frequently found in periodontitis patients, are of unknown pathogenicity but can be associated with thrombosis, stroke, myocardial infarction, and adverse pregnancy outcomes. Principal findings We found that anticardiolipin from periodontitis patients stimulate endothelial cells to produce a cytokine, MCP-1, that is central to the development of atherosclerotic lesions. Practical implications The data indicate that it is possible that these antibodies are pathogenic and could explain some of the associations between periodontitis and systemic diseases. Assessments for anticardiolipin are routine clinical assays, and could be incorporated into a risk profile for these patients. Acknowledgements The authors gratefully acknowledge Kimberly Hollaway for her expert clinical management of the subjects participating in this study. Source of Funding Statement This project was supported in part by grant RO1DE018125 from your National Institute of Dental care and Craniofacial Research. Footnotes Conflict of Interest The authors declare that there are no conflicts SNRNP65 of interest related to this paper..