Immune responses in endocarditis

Brown, Michael L.; Griffin, George E.

doi:10.1136/hrt.79.1.1

Cited by 20 publications

(8 citation statements)

References 18 publications

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“…Accompanied by vegetation formation, the pathogenesis of infective endocarditis is characterized histopathologically by an inflammatory reaction, greatest at the site of attachment or base of the vegetation. The intensity of inflammation and tissue destruction may vary, depending on the bacterial species and clinical onset, classified as acute or subacute, as well as the relative numbers and distribution of inflammatory infiltrate (5,7). Nonetheless, the cellular or bacterial components involved in endocardial inflammation and tissue damage remain unclear.…”

mentioning

confidence: 99%

Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis

Shun¹,

Yeh

et al. 2005

Infect Immun

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The glucosyltransferases (GTFs) of viridans streptococci, common pathogens of infective endocarditis, are extracellular proteins that convert sucrose into exopolysaccharides and glucans. GTFs B, C, and D of Streptococcus mutans are modulins that induce, in vitro and in vivo, the production of cytokines, in particular interleukin-6 (IL-6), from monocytes. The roles of S. mutans GTFs in infectivity and inflammation in situ were tested in a rat experimental model of endocarditis. No significant differences in infectivity, in terms of 95% infective dose and densities of bacteria inside vegetations, were observed between laboratory strain GS-5 and two clinical isolates or isogenic mutant NHS1DD, defective in the expression of GTFs. In aortic valves and surrounding tissues, IL-6 was detected by Western blots and immunostaining 24 h after GS-5 infection, was maintained over 72 h, and was followed by production of tumor necrosis factor alpha but not IL-1␤. Animals infected with NHS1DD showed markedly lower levels of IL-6 (less than 5% of that of parental GS-5-infected rats), while tumor necrosis factor alpha was unaffected. In contrast, animals infected with NHR1DD, another isogenic mutant expressing only GtfB, showed a much smaller reduction (down to 56%). These results suggest that GTFs are specific modulins that act during acute inflammation, inducing IL-6 from endothelial cells surrounding the infected valves without affecting bacterial colonization in vegetations, and that IL-6 might persist in chronic inflammation in endocarditis.

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mentioning

confidence: 99%

Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis

Shun¹,

Yeh

et al. 2005

Infect Immun

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“…Bacteria of low virulence can induce severe disease when present in vegetations. Extracardiac manifestations such as renal lesions, arthritis, vasculitis, splenomegaly, splenic infarcts cutaneous and ocular signs cannot be explained alone by the presence of circulating bacteria (7).…”

mentioning

confidence: 99%

Inflammatory Response in Infective Endocarditis

Deviri

Glenville

2007

Eur J Inflamm

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Endocarditis remains a devastating disease with a high mortality despite timely diagnosis and treatment. The mainstays of treatment include appropriate antibiotics and when indicated, removal of the septic focus. This sounds extremely simple and belies the necessity for a sophisticated multidisciplinary approach to its treatment, the success of which depends not just on the right antibiotic at the right dosage via the right portal, but also on a profound understanding of the inflammatory and infective pathophysiology at work. This review aims at assisting both the clinician and the lab-based physician in the task.

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“…Existing data supports the deposition of circulating immune complexes (CICs) in various target tissues rather than their in situ creation. Immunoglobulin and complement complexes are typically seen with streptococci which are triggering the classic complement pathway, in contrast with antigen and complement deposits observed with staphylococci which are initiating the alternative pathway [71]. CIC concentrations have been associated with hypocomplementaemia, extravalvular lesions and duration of illness.…”

Section: Host Immune Responses In Ivdas Iementioning

confidence: 98%

Dealing with the Substance Abuse Epidemic and Infective Endocarditis:Clinical, Immunologic and Pathogenetic Aspects

Starakis¹,

Panos²,

Mazokopakis

2012

CVP

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Although infective endocarditis (IE) is not the most frequent infection seen in intravenous (IV) drug abusers (IVDAs), health care providers should always regard it as a possible diagnosis in this population. Many researchers have tried to elucidate the clinical, epidemiologic, immunologic and pathogenetic aspects of this entity. Right-sided endocarditis accounts for almost 10% of all IE episodes and has been most commonly interrelated with IV use of illicit substances. On the other hand, recent reports have proposed that left-sided valve participation is seen more often now than in the past. While, our progress in medicine, new diagnostic criteria and especially modern imaging techniques have broadened our ability to recognize IE, there are still some gray areas regarding right-sided IE. Our aim is to comprehensively review the clinical features and complications and also the possible pathogenetic and immunologic mechanisms implicated in IE patients who are injecting illicit substances.

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Immune responses in endocarditis

Cited by 20 publications

References 18 publications

Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis

Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis

Inflammatory Response in Infective Endocarditis

Dealing with the Substance Abuse Epidemic and Infective Endocarditis:Clinical, Immunologic and Pathogenetic Aspects

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