14 DAY TRIAL // In a number of medical studies, the appearance of the chronic obstructive pulmonary disease (COPD) has been directly linked to first-hand smoking, but the scientists conducting the experiments at the time may have missed another important aspect of the effects of tobacco – the fact that it also causes impairments in the immune system, which facilitate the emergence of complications associated with COPD. The new conclusion comes from experts at the McMaster University, who have published their research in the second April issue of the American Journal of Respiratory and Critical Care Medicine.
“It is well established that smoking is the main risk factor for COPD. But our research also suggests that cigarette smoke substantially changes the immune response to bacteria, which means that patients with COPD who smoke are weakening their body's ability to deal effectively with bacterial invaders. This may cause even further progression of the disease,” the principal investigator for the new study, McMaster University Associate Professor Martin Stampfli, PhD, explained.
In the experiments, a group of mice was subjected to cigarette smoke for a period of time roughly comparable with that of an average human smoker. The animals were then inoculated with the Nontypeable Haemophilus influenzae (NTHI), a bacterium that can cause otitis media, sinusitis, pneumonia, conjunctivitis, and, occasionally, septicemia, septic arthritis and meningitis. What's also important to know about it is the fact that NTHI is a normal part of the human respiratory tract.
Another group of mice, formed for control, was not subjected to tobacco smoke, but was also given the bacterium, so as to make the creatures get sick as well. The point of the research is to understand whether or not smoking influences the later development of the disease in “smoking” mice, as opposed to the “healthy” ones. Conclusions show that both those that were exposed to smoke for four days, and for eight weeks, respectively, suffered an increased damage from NTHI, had lost weight due to the bacterial infections, and also that they exhibited a modified biomarker response of the immune system.
“Many interventions are developed with a homeostatic model in mind. However, if our findings are borne out in clinical research, they would indicate that treatment targets for smokers with COPD may be markedly different than in non-smokers. Smoking may change the underlying inflammatory pathways elicited after bacterial infection,” Dr. Stampfli added.
The use of the corticosteroid dexamethasone “raises questions about the long-term use of corticosteroids in COPD. Certainly, there is evidence that corticosteroid treatment reduces the number of exacerbations in patients with COPD. This, however, is associated with occurrence of pneumonia, which is mirrored by our results. Therefore, inflammation is not altogether bad in the context of a bacterial infection, as it is required to clear the bacteria. It is the excessive inflammation observed in smokers that is of concern, as it may lead to lung damage,” the expert concluded.