Dr. Chow and Dr. Matsuda discuss the relationship between pollution and airway inflammation

SOCAAR Seminar Dec. 5, 2012–Air pollution from traffic can trigger or worsen diseases like asthma and chronic rejection following lung transplantation which usually manifest as bronchiolitis obliterans syndrome. Common problems to both diseases are airflow obstruction and airway scarring, likely caused by airway inflammation and abnormal tissue repair from pollution exposure.

In asthma sufferers, the airway muscle thickens and scar tissues forms in the airway. Similarly, in bronchiolitis obliterans syndrome, scarring also occurs but in this case, the scar tissue leads to the obliteration of the airway lumen.

Dr. Chung-Wai Chow, an Assistant Professor in the Division of Respiratory and Multi-Organ Transplant Programme at Toronto General Hospital, spoke about her group’s recent study which identifies spleen tyrosine kinase (Syk), a critical enzyme for regulating the immune system, to play a key role in airway inflammation, cell division and growth, and tissue repair (e.g. wound healing).

The group looked at the airway resistance in asthmatic mice exposed to air pollution. They found that mice with the Syk enzyme either inhibited or deficient did not show enhanced airway resistance, a sign of asthma. Syk mediates the airway response to air pollution, which also means it has an important role in pollution-induced exacerbation of asthma.

The role of Syk in tissue repair was addressed in Dr. Matsuda’s talk. Dr. Matsuda, a Research Fellow and Lung Transplant Clinical Fellow of Latner Thoracic Surgery at the University Health Network, discussed the role of Syk in the airway recovery after the trachea from one mouse was implanted into another mouse’s lung (a mouse model of bronchiolitis obliterans). He showed Syk suppression in mouse models prevented replacement of the airway lumen obliteration by fibrosis, the typical lesion seen in. Syk suppression also lessened the development of lymphoid neogensis, formation of lymph node-like structures, in mice with trachea implants. Lymphoid neogensis has been linked to the chronic inflammation in various chronic inflammatory diseases. In order words, loss of Syk also suppressed chronic inflammation in the mouse trachea transplant model.

These mouse models show that controlling the expression of Syk to be a potential strategy to relieve increase airway hyper-responsiveness in asthma and to prevent chronic rejection of lung transplantation by limiting inflammation and scar formation. Syk is still far from being ready to be used in clinical studies. But Dr. Chow believes that asthma suffers triggered by pollution could one day be using inhalers that contain a Syk inhibitor rather than steroids.

**Watch Dr. Chow’s and Dr. Matsuda’s presentations here**