Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of sialy-Lewis(x) (sLe(x); Neu5Ac alpha 2-3 Gal beta 1-4) (Fuc alpha 1-3) GlcNAc-R) on oral bacteria producing infective endocarditis was determined by a whole-cell enzyme linked immunosorbent assay and an immunoelectron microscopy using the well-characterized anti-sLe(x) monoclonal antibody SNH-3 (mAb SNH-3; IgM class). mAb SNH-3 reacted strongly with whole cells of oral bacteria: Streptococcus sanguis, Streptococcus mutans, Streptococcus mitis, Streptococcus salivarius, Streptococcus intermedius, Streptococcus constellatus, Streptococcus anginosus, Streptococcus pyogenes, Actinobacillus actinomycetemcomitans, Eikenella corrodens and Porphyromonas gingivalis. The negatively stained immuno-electron micrograph of Streptococcus pyogenes showed many reactive gold particles on the cell surface. Our findings demonstrated the existence of immunologic mimicry between the sLe(x) oligosaccharide and cell surface antigens of many species associated with infective endocarditis. We propose the hypothesis that if these bacteria escape their normal habitats, the surface components that mimic the sLe(x) oligosaccharide might bind to host antigens of the selectin family which could promote binding to endothelial cells and, consequently, initiation of the events leading to infective endocarditis.
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PMID:Cross-reactivity between human sialyl Lewis(x) oligosaccharide and common causative oral bacteria of infective endocarditis. 858 66

Rheumatic heart disease is still a relevant problem in children, adolescents and young adults. Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity and tissue damage in rheumatic heart disease. Despite the widespread application of Jones' criteria, carditis is either underdiagnosed or overdiagnosed. Endocarditis leading to mitral and/or aortic regurgitation influences morbidity and mortality of rheumatic heart disease, whilst myocarditis and pericarditis are less significant in determining adverse outcomes in the long-term. Strategy available for disease control remains mainly secondary prophylaxis with the long-acting penicillin G-benzathine.
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PMID:Rheumatic heart disease in children: from clinical assessment to therapeutical management. 1687 42

Cardiovascular disease is on the rise. In India and other developing countries, rheumatic heart disease (RHD) continues to be a major public health problem and contributes to significant cardiac morbidity and mortality. RHD in the juvenile age group namely juvenile mitral stenosis is a variant which is unique to the Indian subcontinent. Severe valve deformities lead to high morbidity and mortality. Despite various measures no appreciable decline in prevalence of RHD has been documented. At autopsy, mitral valve was most commonly affected either alone or in combination with aortic and tricuspid valves. Both functional and organic involvement of tricuspid valve was documented. It has been convincingly demonstrated that molecular mimicry between Streptococcus pyogenes antigen and human proteins lead to autoimmune reactions both humoral and cell mediated causing RF/RHD. Heart tissues namely the valves, left atrial appendage (LAA) and myocardium reveal variable amounts of infiltration by lymphocytes. Significant endocarditis and valvulitis is observed in these cases. CD4+ T cells are most likely the ultimate effectors of chronic valve lesions in RHD. They can recognize Streptococcal M5 protein peptides and produce various inflammatory cytokines such as TNF-alpha, IFN-gamma, IL-10, IL-4 which could be responsible for progressive fibrotic valvular lesions. Cardiac myosin has been defined as a putative autoantigen recognized by autoantibodies of RF patients. Cross reactivity between cardiac myosin and group A beta hemolytic Streptococcal M protein has been adequately demonstrated. Cardiac myosin has been shown to produce myocarditis in rats and mice. Valvulitis/ endocarditis has been observed in excised LAA, cardiac valves and in hearts at autopsy from cases of RHD. The disease predominantly affects the valvular endocardium culminating in crippling valve deformities. Endocardial infiltrate and their migration into the valve substance has been elegantly demonstrated in rats and mice. Immune responses against cardiac myosin lead to valvular heart disease and infiltration of the heart by Streptococcal M protein reactive T lymphocytes. Mitral valves showed various degrees of calcification. An interesting observation is the nature of calcification in diseased/distorted valves in RHD. Recent studies indicate that calcification is not merely an inactive, "dystrophic" process but involves a regulated inflammatory process associated with expression of osteoblast markers and neoangiogenesis. Increased plasma osteopontin levels correlated with severity of mitral valve calcification. Further evidence of inflammation is supported by high levels of advanced oxidation protein products and high sensitive C-reactive protein in plasma detected in patients with RHD. Presence of inflammatory cells and increased expression of several cytokines in cases of "end stage" RHD reflects a possible subclinical, ongoing insult/injury to some unrecognized antigenic stimulus by beta hemolytic Streptococcal antigens that have sensitized/primed the various target tissues and which further culminate in permanent valve deformities.
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PMID:Pathology and pathogenesis of rheumatic heart disease. 1830 30