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Clinical and Vaccine Immunology, June 2008, p. 932-936, Vol. 15, No. 6
1071-412X/08/$08.00+0     doi:10.1128/CVI.00324-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology{triangledown}

Rajendranath Ramasawmy,1,2* Guilherme S. Spina,1 Kellen C. Fae,1,2 Alexandre C. Pereira,1 Renato Nisihara,4 Iara Jose Messias Reason,4 Max Grinberg,1 Flavio Tarasoutchi,1 Jorge Kalil,1,2,3 and Luiza Guilherme1,2

Heart Institute (InCor), University of Sao Paulo School of Medicine, Sao Paulo, Brazil,1 Institute for Investigation in Immunology, Millennium Institutes, Sao Paulo, Brazil,2 Clinical Immunology and Allergy Department, University of Sao Paulo School of Medicine, Sao Paulo, Brazil,3 Department of Clinical Pathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil4

Received 30 July 2007/ Returned for modification 6 November 2007/ Accepted 25 March 2008

N-Acetylglucosamine (GlcNAc) is the major immunoepitope of group A streptococcal cell wall carbohydrates. Antistreptococcal antibodies cross-reactive with anti-GlcNAc and laminin are present in sera of patients with rheumatic fever. The cross-reactivity of these antibodies with human heart valvular endothelium and the underlying basement membrane has been suggested to be a possible cause of immune-mediated valve lesion. Mannose-binding lectin (MBL) encoded by the MBL2 gene, a soluble pathogen recognition receptor, has high affinity for GlcNAc. We postulated that mutations in exon 1 of the MBL2 gene associated with a deficient serum level of MBL may contribute to chronic severe aortic regurgitation (AR) of rheumatic etiology. We studied 90 patients with severe chronic AR of rheumatic etiology and 281 healthy controls (HC) for the variants of the MBL2 gene at codons 52, 54, and 57 by using a PCR-restriction fragment length polymorphism-based method. We observed a significant difference in the prevalence of defective MBL2 alleles between patients with chronic severe AR and HC. Sixteen percent of patients with chronic severe AR were homozygotes or compound heterozygotes for defective MBL alleles in contrast to 5% for HC (P = 0.0022; odds ratio, 3.5 [95% confidence interval, 1.6 to 7.7]). No association was detected with the variant of the MASP2 gene. Our study suggests that MBL deficiency may contribute to the development of chronic severe AR of rheumatic etiology.

* Corresponding author. Mailing address: Heart Institute (InCor), University of Sao Paulo School of Medicine, Laboratory of Immunology, Av. Enéas de Carvalho Aguiar, 44, Bloco II-9° andar, São Paulo, SP 05403-000, Brazil. Phone: 55 11 3069 59 07. Fax: 55 11 3069 59 53. E-mail: ramasawm{at}usp.br

{triangledown} Published ahead of print on 9 April 2008.

Clinical and Vaccine Immunology, June 2008, p. 932-936, Vol. 15, No. 6
1071-412X/08/$08.00+0     doi:10.1128/CVI.00324-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Bocchi, E A, Guimaraes, G, Tarasoutshi, F, Spina, G, Mangini, S, Bacal, F (2009). Cardiomyopathy, adult valve disease and heart failure in South America. Heart 95: 181-189 [Abstract] [Full Text]  


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