The Takeda lab’s mission is to explore the new therapeutic approach to emphysema. Emphysema is the main form of chronic obstructive pulmonary disease (COPD) or alpha-1 antitrypsin deficiency (AATD). Emphysema is a long-term, progressive disease in which the lung tissue is impaired or damaged, and causes shortness of breath. Although this disease condition has been thought to be irreversible, we are investigating the therapeutic effects of mesenchymal stem cell (MSC) and recombinant alpha-1 antitrypsin fused with Fc (AAT-Fc) to repair damaged lung tissue in experimental emphysema. We demonstrated that MSC treatment combined with all-trans retinoic acid dramatically improved damaged lung tissue. Currently, we are investigating the underlying mechanism of this treatment to strengthen the effects. Another research project that is advancing is the investigation of the effects of AAT-Fc on damaged lung tissue in experimental emphysema. As AAT-Fc has an extended half-life compared with plasma-derived AAT (which is currently given to patients with AATD-associated emphysema), dose and frequency of the treatment can be dramatically reduced with this molecule. Thus, the project may be beneficial to AATD patients.

 

Lab Resources and Services

The lab is located on the 9th floor of the Goodman Building. Learn more.

 

Current Projects

 

  • Katsuyuki Takeda
    Katsuyuki Takeda, MD, PhD

Personnel

Principal Investigator

Katsuyuki Takeda, MD, PhD
Associate Professor
303.398.1190
takedak@njhealth.org

Background:

Dr. Takeda was trained as a pulmonologist and later on as an immunologist. His research interests in the last 20 years have focused on the role of airway inflammation in asthma and chronic obstructive pulmonary disease (COPD).

 

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Publications

Takeda K, et al. Eosinophils contribute to the resolution of lung-allergic responses following repeated allergen challenge. J Allergy Clin Immunol. 2015;135:451-460. Abstract

Takeda K, et al. The Critical Role of Complement Alternative Pathway Regulator Factor H in Allergen-Induced Airway Hyperresponsiveness and Inflammation. J Immunol. 2012 188:661-7. 9. Abstract