Asthma - a chronic airway disease affecting roughly 100-150 million people worldwide - is increasing in prevalence and is an important public health concern. It has been recognized for decades that immunological responses in asthma are often similar to those induced by parasitic worm infections, although the link has remained unclear. However, recent research has elucidated that chitinases, enzymes used in pathogen defense against chitin-containing parasitic worms, protozoa, and fungi, play an important role in immune functions and are a characteristic of asthmatic airways.
Recent evidence has elucidated the importance of acidic mammalian chitinase (AMCase), in the inflammatory process of the Th2 pathway in the lungs of asthmatics. Chitinases perform important defensive functions against chitin-containing pathogenic organisms in both the gastrointestinal tract and lungs. Although AMCase is primarily expressed in the gut, and is likely associated with parasitic worm exposure, another chitinase, chitotriosidase (CHIT1), is primarily expressed in the lung. Unlike AMCase, chitotriosidase is induced during Th1 up-regulation, so chitin exposures in the lung should, therefore stimulate Th1 responses. An interesting question, then, is why AMCase is expressed in the lungs of asthmatics.
Human exposure to chitinous pathogens is neither infrequent nor avoidable, even in westernized societies that no longer are parasitized by intestinal helminths. Fungal spores are prevalent in the air we breathe nearly year round, sometimes abundantly so, and pose a constant threat of colonization in the lung. Hence a known insertion/deletion mutation in the Chitotriosidase gene may result in an ineffective chitinase response to fungal or other chitin exposures in the lung. This may precipitate a cascade toward the Th2 pathway in order to up-regulate AMCase as a back-up system and ultimately lead to the asthma phenotype. This presentation reviews recent literature related to this hypothesis.