This release is available in French.
Montreal, June 4th, 2009 – Cigarette smoking induced COPD, or chronic obstructive pulmonary disease, is a disease that results in severe breathing difficulty. According to World Health Organization (WHO) it is the fourth leading killer worldwide. However the mechanisms responsible for some smokers developing COPD and others evading the disease have not been well understood.
Dr.Manuel Cosio from the McGill University Health Centre, in collaboration with Italian and Spanish scientists, reports in the New England Journal of Medicine that an autoimmune mechanism, compounded by genetic predisposition in COPD, would explain the progression of the disease in some smokers and the evasion in others. COPD has a family connection and next of kin of patients with COPD have a much higher chance of developing the disease, a characteristic of autoimmune diseases.
Although smoking is the primary risk factor for COPD in the western world, open fire pollutant cooking and heating fuels in the home is an important risk factor for the development of COPD in women in developing nations. "Smoke can play an important role in autoimmune diseases such as COPD, and other diseases like rheumatoid arthritis, because it accentuates genetic predispositions to the disease," warns Dr. Cosio.
Yet contrary to previous scientific beliefs, COPD does not progress in the same way in all smokers. The authors describe three steps in the potential progression to COPD in smokers: "COPD does not go from stage one, two and three in all people," Dr. Cosio says. "Depending on their personal balance between immune response and immune control some people would stop at stage one, others at stage two, and some will progress to stage three, full autoimmunity and lung destruction."
"Hopefully investigators will now see the disease in a totally different way," Dr Cosio stresses. "Our hope is that our research will open the door for a different investigation on COPD, where scientists learn more about the immunological processes and how these processes could be controlled and modulated to eventually provide the right treatment."
Dr Manuel Cosio
Dr Manuel Cosio is Professor of respiratory medicine at the McGill University Health Centre (MUHC) and an investigator in "Respiratory health" at the Meakins Christie laboratories of the Research institute of the MUHC.
Funding
This study was supported by the Lloyd-Carr Harris Foundation, the Italian Ministry of University and Research and CIBERES (Centro de investigación biomédica en red sobre enfermedades respiratorias).
Partners
This article was authored by Dr.Manuel G. Cosio of the McGill University Health Centre (Canada), Dr.Marina Saetta of the University of Padua, (Italy) and Dr.Alvar Agusti of the Hospital Universitario Son Dureta, (Spain).
The Research Institute of the McGill University Health Centre (RI MUHC) is a world-renowned biomedical and health-care hospital research centre. Located in Montreal, Quebec, the institute is the research arm of the MUHC, the university health center affiliated with the Faculty of Medicine at McGill University. The institute supports over 600 researchers, nearly 1200 graduate and post-doctoral students and operates more than 300 laboratories devoted to a broad spectrum of fundamental and clinical research. The Research Institute operates at the forefront of knowledge, innovation and technology and is inextricably linked to the clinical programs of the MUHC, ensuring that patients benefit directly from the latest research-based knowledge.
The Research Institute of the MUHC is supported in part by the Fonds de la recherche en santé du Québec.
For further details visit: www.muhc.ca/research.
Journal
New England Journal of Medicine