CVI Accepts, published online ahead of print on 9 April 2008

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Clin. Vaccine Immunol. doi:10.1128/CVI.00324-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. 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

Rajendranath Ramasawmy^*, Guilherme S. Spina, Kellen C. Fae, Alexandre C. Perreira, Renato Nisihara, Iara Jose Messias Reason, Max Grinberg, Flavio Tarasoutchi, Jorge Kalil, and Luiza Guilherme

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

^* To whom correspondence should be addressed. Email: ramasawm{at}usp.br.

Background – N-acetylglucosamine (GlcNAc) is the major immunoepitope of group A streptococcal cell wall carbohydrates. Anti-streptococcal 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 the exon I of MBL2 gene associated with deficient serum level of MBL may contribute to chronic severe aortic regurgitation (AR) of rheumatic etiology.

Methods – We studied 90 patients with severe chronic AR of rheumatic etiology and 281 healthy controls (HC) for the variants of MBL2 gene at codon 52, 54 and 57 by a PCR-RFLP based method.

Results –We observed a significant difference in the prevalence of deficient MBL2 alleles between patients with chronic severe AR and HC. 16% of patients with chronic severe AR were homozygote or compound heterozygote for deficient MBL alleles in contrast to 5% for HC (P=0.0022; OR=3.5 [95%CI 1.6 – 7.7]). No association was detected with the variant of the MASP2 gene.

Conclusion –Our study suggests that MBL deficiency may contribute to the development of chronic severe AR of rheumatic etiology.

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