Asthma is a chronic inflammatory disease characterized by airway
inflammation, mucus hypersecretion and
airway hyperresponsiveness. Mechanisms underlying the pathogenesis of
asthma are not fully understood. In recent years, there are mounting evidences demonstrating that mammalian
chitinases may play a key role in mediating the T-helper 2 cell-driven inflammatory response that is commonly associated with
asthma.
Chitinases (e.g.,
chitotriosidase and acidic mammalian
chitinase) are
enzymes that degrade
chitin, the second most abundant
biopolymer that can be found in the cell walls of fungi, microfilarial sheaths of helminths, and exoskeletons of insects and crustaceans. There are also
chitinase-like
proteins (e.g., YKL-40, Ym1 and Ym2) that lack chitinolytic activity but retain
chitin-binding ability. Therefore,
chitinases were originally believed to function in host defense against
parasitic infections, but the first discovery of their role in inflammatory airway diseases came as a surprise. There is ample evidence to support an association of acidic mammalian
chitinase and YKL-40 with allergic
bronchial asthma in patients. Our recent studies in a mouse
asthma model revealed that anti-inflammatory drugs like
corticosteroid and
cysteinyl leukotriene receptor antagonist were able to suppress elevated pulmonary levels of mammalian
chitinases. Taken together, mammalian
chitinases may be useful as
biomarkers for
asthma. Notwithstanding, large-scale multi-center association studies are required to confirm this hypothesis. Besides, substantially more works using knockout mice, recombinant
chitinases and
siRNA technology are required to investigate a potential role of
chitinases in the pathogenesis of
asthma.