Chronic obstructive pulmonary disease (COPD) are very common global diseases as both are increasing and have an enormous impact on the lives of patients and their careers.COPD has become a global epidemic, which is increasing as populations age and survive previous causes of death.In developed countries the predominant risk factor for developing COPD is cigarette smoking and it now affects women as often as men, reflecting the equal prevalence of smoking. In low and middle income countries, COPD is often seen in non-smokers and due to wood smoke (biomass) exposure.Unlike asthma, the inflammation in COPD is predominantly localized to peripheral airways and lung parenchyma and is also associated with systemic inflammation.
In COPD there is an increase in neutrophils and macrophages in the airway lumen and greater numbers of macrophages, T lymphocytes and B lymphocytes in the airway wall and parenchyma, Resistance to the anti-inflammatory effects of corticosteroids is one of the major barriers to effective treatment of severe asthma and COPD, prompting a search for alternative anti-inflammatory treatments. Several molecular mechanisms of corticosteroids in COPD have been identified and include decreased HDAC2 activity and expression due to activation of PI3K signalling pathways in severe asthma and COPD, phosphorylation of the glucocorticoid receptor (GR) by MAP kinases, such as p38 and JNK, which reduce GR nuclear translocation and activation of mammalian target of rapamycin (mTOR), resulting in increased c-Jun and increased activation of transcription factor activator protein-1 (AP-1).

References

1.Peter J. Barnes . Clinical Science (2017) 131 1541–1558.