To be sure that the lungs are functioning properly, the white blood cells called macrophages, remove the debris and bacteria that can build up in the lungs and cause infection.
Now, researchers have figured out that a chemical pathway in the lungs called NRF2, involved in macrophage activation, is wiped out by smoking. They also found that sulphoraphane, a plant chemical that is made by broccoli, cauliflower and other cruciferous vegetables when damaged, such as when chewed, can restore this pathway.
This cleaning system is defective in smokers and people with chronic obstructive pulmonary disease (COPD) – a combination of emphysema and bronchitis – who suffer from frequent infections.
At Johns Hopkins University in Baltimore, Maryland, Shyam Biswal and his colleagues exposed defective macrophages from the lungs of 43 people with COPD in two bacterial species that are common causes of COPD-related infections. In the presence of sulforaphane, NRF2-was boosted by the ability of macrophages to recognize and engulf bacteria is restored.
They researched with mice. They were exposed to cigarette smoke for a week or six months. Increased bacterial colonization of the lungs was found in them, similar to COPD. After treating the mice with sulphoraphane, they found that the bacteria were reduced. Instead of activating the macrophages, sulphoraphane has been shown to improve the functionality of the cells.
Sulphoraphane is present in broccoli in its precursor form and is converted to the active compound by enzymes present in saliva and intestinal bacteria, says Christopher Harvey, co-author of the research.
Levels of the enzyme are different inpeople, which mean it can be expected that the dose of sulforaphane derived diet will vary between people. Further studies established beneficial effects of sulforaphane diet rich in immune defense, he says.Biswal says he needs three years to obtain information on how to improve the function of the lungsin humans. The team has started Phase 2 clinical tests, testing the compound in people with COPD. “There are many diseases that have defective lung function as a result of increased bacterial function in the lungs,” he says, “so this study can be extrapolated to those diseases too.”