NIH COPD clinical trials

COPD is the third leading cause of death nationwide. It’s often brought on by cigarette smoking. COPD can cause shortness of breath, wheezing and coughing, among other symptoms. In patients with COPD, immune cells called macrophages lose their ability to engulf and remove bacteria, making the lungs more vulnerable to infection. Infection can lead to inflammation, which is a major cause of impaired lung function and death in these patients. Until now, no one knew how to reverse this damage to the macrophages.

A team of scientists at Johns Hopkins University, led by Drs. Shyam Biswal and Robert Wise, investigated why macrophages don’t work properly in COPD patients. Previous research suggested that a process called oxidative stress might be to blame. Oxidative stress occurs when the body can’t effectively neutralize damaging compounds called peroxides and free radicals.

A molecule called Nrf2 can cause cells to make more antioxidants, which neutralize these harmful compounds. Previous studies found reduced Nrf2 activity in severe COPD. The scientists suspected that increasing Nrf2 activity might restore the ability of macrophages to remove bacteria. To test their theory, the team used a chemical called sulforaphane, which is known to activate Nrf2. A precursor of sulforaphane is found in broccoli. The research was cosponsored by NIH’s National Heart, Lung and Blood Institute (NHLBI) and National Institute of Environmental Health Sciences (NIEHS). The results appeared in the April 13, 2011, issue of Science Translational Medicine.

The researchers first took macrophages from the lungs of patients with moderate COPD. When they treated these macrophages with sulforaphane, they saw higher Nrf2 levels in the cells. Sulforaphane treatment also boosted the ability of cultured macrophages to clear 2 of the major types of bacteria that infect COPD patients. Macrophage uptake of bacteria rose 300% after treatment, whether the cells came from smokers or non-smokers.

Photo of broccoli.

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