Chronic obstructive pulmonary disease (COPD) leads to persistent inflammation of the airways and is typically managed with corticosteroids, a class of anti-inflammatory medication. However, corticosteroids do not improve survival nor alter the progression of COPD and may reduce lung symptoms as little as 20 percent.
Image of COPD in X-Rays Chest
A new study led by researchers at the Johns Hopkins Bloomberg School of Public Health, found why corticosteroids do not work well for COPD patients and additional treatment with sulforaphane—an ingredient of broccoli and other vegetables—can improve the effectiveness of corticosteroids. The study was published online October 17, 2011, in advance of print in the Journal of Clinical Investigation.
Exacerbations of the disease occur due to super-added infections and inflammation that increases the obstruction to breathing. It has been seen that nitrosamine in cigarette smoke causes S-nitrosylation of of Histone Deacetylase 2 (HDAC2).
HDAC2 takes a critical part in the chain reaction to enable corticosteroids to reduce inflammation. S-nitrosylation causes HDAC2 dysfunction and leads to corticosteroid insensitivity in the alveolar defence by macrophages (White blood Cells) of the lungs of individuals with COPD. This also cases defect in phagocytosis, a process of uptake of the offending bacteria by the macrophages. HDAC2 is substantially reduced in the lung tissue of individuals with COPD.
Restoring corticosteroid sensitivity in patients with COPD by targeting the Nrf2 pathway holds promise for effectively treating exacerbations. This molecule is found in broccoli, cabbage and other cruciferous vegetables.
Image of COPD in X-Rays ChestA new study led by researchers at the Johns Hopkins Bloomberg School of Public Health, found why corticosteroids do not work well for COPD patients and additional treatment with sulforaphane—an ingredient of broccoli and other vegetables—can improve the effectiveness of corticosteroids. The study was published online October 17, 2011, in advance of print in the Journal of Clinical Investigation.
Exacerbations of the disease occur due to super-added infections and inflammation that increases the obstruction to breathing. It has been seen that nitrosamine in cigarette smoke causes S-nitrosylation of of Histone Deacetylase 2 (HDAC2).
HDAC2 takes a critical part in the chain reaction to enable corticosteroids to reduce inflammation. S-nitrosylation causes HDAC2 dysfunction and leads to corticosteroid insensitivity in the alveolar defence by macrophages (White blood Cells) of the lungs of individuals with COPD. This also cases defect in phagocytosis, a process of uptake of the offending bacteria by the macrophages. HDAC2 is substantially reduced in the lung tissue of individuals with COPD.
The study showed that sulforaphane could increase expression of receptors that improve macrophage phagocytic function. Sulphorafane activates Nrf2 (nuclear factor erythroid 2–related factor 2) pathwayand restores the ability of macrophages to phagocytose the bacteria and clear lungs of the organisms.
Furthermore, the research team found that treatment with sulforaphane restored HDAC2 activity and corticosteroid sensitivity.
Restoring corticosteroid sensitivity in patients with COPD by targeting the Nrf2 pathway holds promise for effectively treating exacerbations. This molecule is found in broccoli, cabbage and other cruciferous vegetables.
