Chu Laboratory

Our lab’s mission is to understand the mechanisms of airway bacterial infections in patients with asthma or COPD, and to discover novel therapeutic approaches to restore host defense functions. We have identified impaired Toll-like receptor 2 (TLR2) signaling, and reduced production of host defense molecule short palate, lung, and nasal epithelium clone 1 (SPLUNC1) in allergic airways. Furthermore, we have found that cigarette smoke exposure dampens airway epithelial innate immune responses to bacteria such as Mycoplasma pneumonaie and Moraxella catarrhalis.

 

Lab Resources and Services

The Chu Laboratory offers several unique research methods and animal models for pulmonary basic science research. Learn more.

 

Current Projects

• Effects of Allergic Inflammation on TLR2 Signaling and Mycoplasma Infection
• SPLUNC1 Protein in Host Defense Against Mycoplasma Pneumoniae Infection
  • Supplement
• Host Defense Functions of Airway Epithelial Cells in COPD

 

Personnel

• Principal Investigator
  Hong Wei Chu, MD
• Instructors
  Qun Wu, MD, PhD
• Lab Researchers
  Reena Berman
  Di Jiang
• Research Associate

           Chunjian Huang
 

Collaborators

Publications

Chu HW, Gally F, Thaikoottathil J, Janssen-Heininger YM, Wu Q, Zhang G, Reisdorph N, Case S, Minor M, Smith S, Jiang D, Michels N, Simon G, Martin RJ. SPLUNC1 regulation in airway epithelial cells: role of Toll-like receptor 2 signaling. Respir Res. 2010 Nov 5;11(1):155. Abstract

Michels NM, Chu HW, Lafasto SC, Case SR, Minor MN, Martin RJ. Mast cells protect against airway Mycoplasma pneumoniae under allergic conditions. Clin Exp Allergy 2010;40:1406-1413. Abstract

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