Immune system may worsen chronic lung diseases in smokersFebruary 10th, 2009 - 5:18 pm ICT by ANI
Washington, Feb 10 (ANI): The immune system of smokers with chronic lung diseases can backfire, and actually worsen their condition, according to new University of Cincinnati (UC) research.
In the pre-clinical study, UC environmental health scientists found that activation of a specific cellular receptor (NKG2D) critical to immune system activation is linked with cigarette smoke.
This association could worsen one of the most difficult-to-treat respiratory diseases: chronic obstructive pulmonary disorder (COPD), said the researchers.
They said that the finding was key to understanding COPD disease progression, and developing future interventional drug therapies.
“People have historically believed that if you smoke, you suppress the immune system. We”ve shown that you actually activate certain parts of the immune system and it could potentially work against you,” said Dr. Michael Borchers, lead investigator of the study and UC assistant professor of environmental health.
COPD is a progressive pulmonary disease believed to be caused by long-term cigarette smoking, and is characterised by emphysema and severe inflammation of the lung tissue.
It was found in earlier research that immune cells (lymphocytes) contributed to chronic inflammation, a key indicator of COPD, but it was unclear whether this caused extensive cellular damage.
Thus, the researchers developed a transgenic mouse model to further examine how the immune system responds to chronic inflammation indicative of COPD.
They hypothesized that when tissue was damaged, the cells would send signals to the immune system indicating they are transformed-similar to cancer or virally infected cells-and must be destroyed.
After examining molecular signalling pathways in lung tissue exposed to cigarette smoke, the scientists found a strong correlation between cellular stress signals, activation of the immune system and development of COPD-like disease.
The method was repeated and cross-referenced in tissue samples from a human cohort that included non-smokers, smokers with COPD and smokers who did not develop COPD.
In patients who had never smoked, there was a complete absence of the NKG2D signal. Current and former smokers who developed the disease expressed signals that correlated with severe COPD disease.
Thus, they concluded that cigarette smoke set off a molecular chain of events resulting in activation of a specific receptor-NKG2D-in lung cells, causing the immune system to attack stressed (damaged) lung tissue.
“Our study is evidence that when the lungs are exposed to chronic damage from cigarette smoke, at some point that damage exceeds the body’’s natural ability to repair tissue and can start to contribute to COPD instead of protecting against it,” said Borchers.
The researchers report their findings in the March 2009 issue of the Journal of Clinical Investigation. (ANI)
- Protein shows promise in treating smoker's diseases - Jan 16, 2012
- e-cigarettes damaging lungs? - Sep 03, 2012
- Protein involved in cystic fibrosis linked to chronic lung diseases - Dec 30, 2010
- Smoking plus exposure to wood smoke increases risk of COPD - Jul 16, 2010
- New therapeutic target for asthma, other lung disorders identified - Apr 18, 2011
- Protein that contributes to ulcerative colitis revealed - Apr 02, 2011
- Lung cancer mostly diagnosed late (Nov 17 is World Lung Cancer Day) - Nov 17, 2011
- Passive smoking doing more harm than people may think - Aug 21, 2010
- Enzyme essential for healthy lung development discovered - Mar 30, 2011
- Ciggie smoke 'weakens lungs' natural defense against harmful pathogen' - Oct 24, 2009
- New way to halt lung inflammation in animal models discovered - Jan 15, 2011
- Cigarette smoke may cause inflammation through a new chemical pathway - Sep 03, 2010
- Cigarette smoking ups production of mucus in patients with bronchitis - Feb 18, 2011
- Re-engineered toxins can treat asthma, arthritis - Jan 02, 2012
- Regular use of vitamin E may cut COPD risk - May 17, 2010
Tags: borchers, cellular damage, cellular receptor, chronic inflammation, chronic lung diseases, chronic obstructive pulmonary disorder, cigarette smoke, cigarette smoking, earlier research, environmental health scientists, immune cells, immune system activation, lung tissue, parts of the immune system, respiratory diseases, stress signals, transgenic mouse model, uc research, university of cincinnati, virally infected cells