Genetics play a role in the development of COPD.  It is more common among relatives of those with COPD who smoke than unrelated smokers.  Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT).  This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes.  It is responsible for about 1–5% of cases   and the condition is present in about 3–4 in 10,000 people.  Other genetic factors are being investigated,  of which there are likely to be many. 
It’s therefore natural to think of antibiotic therapy as the natural opposite of steroids, and this has some truth to it. In the case of infection — which, remember, is not the only cause of inflammation — steroids do inhibit the immune response. But bear in mind that antibiotics do not, as a general rule, actually support or promote the body’s inflammatory response; rather, they work independently by attacking the infection directly along their own pathways. The result is that some pathologies (such as the contentious cases of sepsis and epiglottitis) may respond both to steroids — to manage the excessive inflammatory response — and antibiotics — to help eliminate the source infection.