SELECTED ARTICLES FROM THE RECENT LITERATURE 2008

4/23/08

Chitin and Asthma

Summary
Chitinase and the chitinase-like protein, YKL-40, have been shown to be elevated in asthma. The authors looked at levels of chitinase-like protein, YKL-40, which binds to but does not digest chitin, in the sera of patients with asthma, and carried out a genomewide association study of YKL-40 levels in a founder population of European descent, the Hutterites.

They tested for an association between a single-nucleotide polymorphism in the gene for YKL-40 to discern whether or not there was a relationship between polymorphisms and asthma. They found that promoter single-nucleotide polymorphism (SNIP) in CH13L1, the chitinase 3-like 1 gene encoding YKL-40, was associated with elevated YKL-40 levels. In addition, this SNIP was found in a population at risk for asthma, bronchial hyperresponsiveness, and lowered pulmonary function in the Hutterites. The same single-nucleotide polymorphism could be used to predict the presence of asthma in the two case-control populations evaluated.

They concluded that CH13L1 is a susceptibility gene for asthma, bronchial hyperresponsiveness, and reduced lung function, and elevated circulating YKL-40 levels are a biomarker for asthma and an exaggerated decline in lung function.

Editor's Comments
Previously, these authors demonstrated that YKL-40 levels were elevated in patients with asthma, and correlated with severity of the disease, thickness of the subepithelial basement membrane, and pulmonary function. In this study, they identified a single-nucleotide polymorphism in chitinase that was a marker for asthma.

An accompanying editorial (Moffatt M, et al. New England Journal of Medicine 2008; 358(16):1725-1726), stated that a likely interpretation of these results support a "causal role of YKL-40, suggesting that the protein directly influences the asthmatic process."

Reference
Ober C, et al. Effect of variation in CH13L1 on serum YKL-40 level, risk of asthma, and lung function. New England Journal of Medicine 2008; 358(16):1683-1691.

 

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