Pulmonary cryptococcosis induces chitinase in the rat

Alfin G Vicencio¹ , Swati Narain² , Zhongfang Du¹ , Wang Yong Zeng² , James Ritch¹ , Arturo Casadevall³ and David L Goldman²^,3

¹Department of Pediatrics, Division of Respiratory and Sleep Medicine, Albert Einstein College of Medicine and Children's Hospital at Montefiore, Bronx, USA

²Department of Pediatrics, Division of Infectious Diseases, Albert Einstein College of Medicine and Children's Hospital at Montefiore, Bronx, USA

³Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, USA

author email corresponding author email

Respiratory Research 2008, 9:40doi:10.1186/1465-9921-9-40


Published:	15 May 2008

Abstract

Background

We previously demonstrated that chronic pulmonary infection with Cryptococcus neoformans results in enhanced allergic inflammation and airway hyperreactivity in a rat model. Because the cell wall of C. neoformans consists of chitin, and since acidic mammalian chitinase (AMCase) has recently been implicated as a novel mediator of asthma, we sought to determine whether such infection induces chitinase activity and expression of AMCase in the rat.

Methods

We utilized a previously-established model of chronic C. neoformans pulmonary infection in the rat to analyze the activity, expression and localization of AMCase.

Results

Our studies indicate that intratracheal inoculation of C. neoformans induces chitinase activity within the lung and bronchoalveolar lavage fluid of infected rats. Chitinase activity is also elicited by pulmonary infection with other fungi (e.g. C. albicans), but not by the inoculation of dead organisms. Enhanced chitinase activity reflects increased AMCase expression by airway epithelial cells and alveolar macrophages. Systemic cryptococcosis is not associated with increased pulmonary chitinase activity or AMCase expression.

Conclusion

Our findings indicate a possible link between respiratory fungal infections, including C. neoformans, and asthma through the induction of AMCase.