High-producing MBL2 genotypes increase the risk of acute and chronic carditis in patients with history of rheumatic fever

Schafranski, Marcelo Derbli; Ferrari, Lilian Pereira; Scherner, Daniela; Torres, Renato Pedro de Almeida; Jensenius, Jens Christian; Messias-Reason, Iara José de

doi:10.1016/j.molimm.2008.05.013

Cited by 43 publications

(44 citation statements)

References 17 publications

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“…This study found that the mean level of MBL was higher in children with RHD compared to healthy children, 1211 ± 14 ng/mL vs 906.6 ± 7 ng/mL. Some previous studies also showed increased levels of MBL in RHD [3,4,18].…”

Section: Discussionmentioning

confidence: 53%

“…The high level of MBL in chronic RHD patients reinforces the presence of chronic inflammation activity contributing to valvular damage via complement activation in RHD patients [3]. Subsequent studies confirmed that high MBL level (> 2.80 ng/mL) increased the risk of chronic RHD (OR 2.91) compared to healthy control [4].…”

Section: Discussionmentioning

confidence: 73%

“…Mannose-binding lectin binds to the surface of the pathogen and has a major role in the innate immune response through the ability to increase opsonization pathogens and activating the complement cascade via the lectin pathway [2]. Previous study showed that there was an increase of MBL level in adult chronic RHD patients, which led to the speculation that the MBL caused complement activation contributing to the pathogenesis of RHD [3,4]. However there has been no study examining the correlation between MBL levels and the severity of valvular regurgitation and heart failure in pediatric RHD.…”

mentioning

confidence: 99%

“…Myeloperoxidase is an important contributor to oxygen-dependent tissue damage in autoimmune and chronic inflammatory diseases [12]. It is known that there were chronic inflammation and autoimmune reaction in the case of rheumatic fever [4]. Until now, there was no study that examined the MPO level in pediatric RHD patients and the relationship of MPO level and the severity of valvular regurgitation and heart failure in pediatric RHD patients.…”

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confidence: 99%

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Prominently Increased of Mannose Binding Lectin (MBL) and Myeloperoxidase (MPO) Levels in Severe Valve Regurgitation and Heart Failure of Rheumatic Heart Disease

Rachmania

Suwarniaty

Fitri

et al. 2017

JTLS

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Rheumatic heart disease (RHD) is mediated by an abnormal immunological response following a Streptococcus pyogenes infection that induces a disturbance of oxidants and antioxidants balances. Mannose-binding lectin (MBL) binds to N-acetylglucosamine, a molecule present on the Streptococcus cell wall and human heart valves. There is a disturbance of oxidant and antioxidant balance in rheumatic disease. Myeloperoxidase (MPO) is a marker of oxidative stress and inflammation. This study was aimed to determine the correlation of MBL and MPO levels and severity of valvular regurgitation and heart failure (HF) in RHD patients. A case-control study was conduct using human peripheral blood samples from 32 children aged 6 to 14 years old. The subjects were divided into two groups: 16 RHD patients included in the case group and 16 healthy children as a control group. The level of MBL and MPO was investigated using ELISA method. There were significant differences on MBL and MPO level between patient and control group. The level of MBL and MPO were significantly increased in RHD group, especially on severe valvular regurgitation. There was a strong correlation between MBL and MPO levels and the severity of valvular regurgitation (r = 0.94 and r = 0.88). The least significant difference (LSD) analysis showed that significant difference occurs in the severe heart failure group. Our research revealed that the MBL and MPO levels in pediatric RHD patients were significantly higher than in healthy children. The MBL and MPO levels were significantly correlated with the severity of valvular regurgitation and heart failure.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 73%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Prominently Increased of Mannose Binding Lectin (MBL) and Myeloperoxidase (MPO) Levels in Severe Valve Regurgitation and Heart Failure of Rheumatic Heart Disease

Rachmania

Suwarniaty

Fitri

et al. 2017

JTLS

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“…Patients with RHD and mitral stenosis have been shown to have an increased incidence of the MBL 'A' allele, which results in higher levels of MBL production, as opposed to the 'O' allele, which yields lower levels. 20,21 The end result is an exaggerated complement activation that likely leads to greater valve inflammation and damage.…”

Section: Genetic Predispositionmentioning

confidence: 99%

The immunology of mitral valve stenosis

Artola¹,

Mihos²,

Santana³

2011

IJICMR

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Although the prevalence of rheumatic heart disease (RHD) has rapidly subsided over the last several decades in the United States, it still remains a serious cardiovascular disorder across the world, particularly in developing nations. Chronic autoimmune inflammation of the cardiac valves can result in mitral stenosis, increasing the risk of morbidity, mortality, and long-term sequelae in these patients. Researchers have begun to unravel the mysteries behind the development of RHD in the setting of chronic autoimmune inflammatory reactions and the roles genetic predisposition, antibody-and T-cell-mediated molecular mimicry, and cytokine proinflammatory responses play. In this article, the immunologic pathogenesis of RHD and its effects on the mitral valve are reviewed.

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Genetic variants in rheumatic fever and rheumatic heart disease

Muhamed

Shaboodien

Engel

2020

American J of Med Genetics Pt C

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Genetic association studies in rheumatic heart disease (RHD) have the potential to contribute toward our understanding of the pathogenetic mechanism, and may shed light on controversies about RHD etiology. Furthermore, genetic association studies may uncover biomarkers that can be used to identify susceptible individuals, and contribute toward developing vaccine and novel therapeutic targets. Genetic predisposition to rheumatic fever and RHD has been hypothesized by findings from familial studies and observed associations between genes located in the human leukocyte antigens on chromosome 6p21.3 and elsewhere in the genome. We sought to summarize, from published Genetic association studies in RHD, evidence on genetic variants implicated in RHD susceptibility. Using HuGENet™ systematic review methods, we evaluated 66 studies reporting on 42 genes. Existing meta‐analyses of candidate gene studies suggest that TGF‐β1 [rs1800469], and IL‐1β [rs2853550] single nucleotide polymorphisms (SNPs) contribute to susceptibility to RHD, whereas the TNF‐α [rs1800629 and rs361525], TGF‐β1 [rs1800470 and rs4803457], IL‐6 [rs1800795], IL‐10 [rs1800896] were not associated with RHD. However, candidate gene studies in RF/RHD are relatively small, thus lacking statistical power to identify reliable and reproducible findings, emphasizing the need for large‐scale multicenter studies with different populations.

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High-producing MBL2 genotypes increase the risk of acute and chronic carditis in patients with history of rheumatic fever

Cited by 43 publications

References 17 publications

Prominently Increased of Mannose Binding Lectin (MBL) and Myeloperoxidase (MPO) Levels in Severe Valve Regurgitation and Heart Failure of Rheumatic Heart Disease

Prominently Increased of Mannose Binding Lectin (MBL) and Myeloperoxidase (MPO) Levels in Severe Valve Regurgitation and Heart Failure of Rheumatic Heart Disease

The immunology of mitral valve stenosis

Genetic variants in rheumatic fever and rheumatic heart disease

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