ArticlePloS one2014
Genetic variants in genes of the inflammatory response in association with infective endocarditis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Inflammatory Response Genes' Polymorphism Associated with Risk of Rheumatic Heart Disease.Journal of personalized medicine · 2024Article
- Case report: Aortic valve endocarditis and recurrent pulmonary valve stenosis.Journal of cardiothoracic surgery · 2023Article
- Neutrophil-Lymphocyte Ratio in Predicting Infective Endocarditis: A Case-Control Retrospective Study.Mediators of inflammation · 2020Article
- Human genetic variation in GLS2 is associated with development of complicated Staphylococcus aureus bacteremia.PLoS genetics · 2018Article
- (3R)-5,6,7-trihydroxy-3-isopropyl-3-methylisochroman-1-one reduces lipoteichoic acid-induced damage in rat cardiomyoblast cells.Anatolian journal of cardiology · 2018Article
- Human Genetic Susceptibility to Native ValveFrontiers in microbiology · 2018Article
- Whole-genome sequencing of bloodstream Staphylococcus aureus isolates does not distinguish bacteraemia from endocarditis.Microbial genomics · 2017Article
- Strain-dependent interactions of Streptococcus gallolyticus subsp. gallolyticus with human blood cells.BMC microbiology · 2017Article
- Inherited Variation in Cytokine, Acute Phase Response, and Calcium Metabolism Genes Affects Susceptibility to Infective Endocarditis.Mediators of inflammation · 2017Article
- Genetics of serum concentration of IL-6 and TNFα in systemic lupus erythematosus and rheumatoid arthritis: a candidate gene analysis.Clinical rheumatology · 2015Article
- Cytokine Signature in Infective Endocarditis.PloS one · 2015Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsInflammation in infective endocarditis (IE) is a complex network including interactions of inflammatory cytokines and other components of host response. Certainly, any variation in this network could influence susceptibility or disease progression of IE. In this study, 14 single nucleotide variants (SNVs) in genes coding for interleukin-1β, interleukin-6, interleukin-10, toll-like receptor-4, tumor necrosis factor-α, selectin E and intercellular adhesion molecule-1 were analyzed for an association with susceptibility to IE and correlated with disease-related laboratory parameters. Furthermore, the occurrence of SNVs was examined to elucidate pathogen-dependent associations. METHODS AND
resultsThe distribution of SNVs was determined in IE-patients and healthy blood donors by RFLP analysis. White blood cells (WBC) were counted using flow cytometry, concentration of C-reactive protein and procalcitonin was measured immunologically. Interleukin-6 c.471+870G>A genotypes differed significantly between IE patients and controls. The frequency of the heterozygote genotype GA was considerably higher in the patient group (68.9% vs. 43.8%, Pc<0.0003). Interleukin-6 c.-237 minor allele frequency was increased in patients, although not statistically significant. Additionally, we detected a potential relation between interleukin-1β c.315C>T and IE. Pathogen-dependent analysis showed no significantly associated subgroup in relation to IE susceptibility, but gave hints towards alterations regarding Enterococcus-caused IE cases. Patients with genotype selectin-E c.-19 GT tend to have higher preoperative WBC counts than patients with genotype GG. We further showed an association between two interleukin-1β SNVs and laboratory biomarkers.
conclusionThis study shows genetic predispositions for the establishment of IE. Furthermore, correlation of SNVs with disease-related biomarkers suggests a role of genetic variants regarding the inflammatory response in IE.
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