Dr. Xiaoping Zhu's Laboratory

Dr. Xiaoping Zhu's research:

Allergic airway inflammations, such as asthma, are an increasingly important disease caused by bronchial inflammation and characterized by bronchial hyper-responsiveness and intermittent airway obstruction with an underlying Th2 cell-biased inflammatory response in the airways of both animals and humans. The disease is currently treated with bronchodilators or anti-inflammatory drugs such as corticosteroids, leukotriene modifiers, and anti-IgE therapy, etc. However, the current treatments are not curative, and some patients do not respond well to intense anti-inflammatory therapies. Additionally, the use of long-term steroids may result in many undesired side effects. For this reason, novel and more effective intervening strategies are greatly needed and explored. Targeting the functions of Th2 cells and their products has been proposed as an effective strategy for the development of potential stand-alone treatments for allergic asthma. The reduction or elimination of allergen specific Th2 cells in early disease development is expected to reduce the consequences of repeated allergic inflammation. Hence, efficient delivery of immunotherapeutic proteins into the airway tract could effectively and directly interfere with allergen specific Th2 cell activation in its earliest phase of function. However, the polarized epithelial monolayer lining the airway forms a mucosal barrier which is impervious to macromolecule diffusion. This barrier poses a major difficulty for the efficient delivery of immunotherapeutic proteins to access and crosstalk with underlying immune effector cells, such as Th2 cells, in the airway. Dr. Xiaoping Zhu’s laboratory has shown that the human CD23 receptor is functionally capable of transporting IgE antibodies across human lung and bronchial epithelial cells. In the current, his laboratory is exploring the feasibility of CD23 to deliver the immunotherapeutic proteins, which are targeted to interfere with CD4+ Th2 cell function, across the airway mucosal barrier in a mouse severe asthma model. These studies, therefore, are very likely to lead to greatly improved novel therapies that protect against and potentially cure severe asthma and allergic diseases.