Smoking remains a widespread habit, despite the fact that its negative effects on health are well recognized. However, until now it was unknown exactly how cigarette smoke causes serious respiratory diseases, which has made the development of effective treatments extremely difficult.
But a group of Australian researchers explains in a study published in ‘Journal of Experimental Medicine‘ (JEM) how multiple chemicals present in cigarette smoke and e-cigarettes alter the function of a key type of immune cell found in the lungs.
The study suggests that these alterations make cigarette smokers and those exposed to second- and thirdhand smoke more susceptible to respiratory infections and worsen smoking-related inflammatory diseases, such as chronic obstructive pulmonary disease (COPD).
Cigarette smoking is known to impair the immune system’s response to infections and promote inflammation in the lungs, which can cause or exacerbate COPD, the third leading cause of death worldwide. Patients with COPD are more susceptible to flu infections, which, in turn, can worsen the underlying disease by increasing airway inflammation and promoting the destruction of lung alveoli. There are currently no effective treatments for COPD.
“Until now, the mechanisms underlying biased immune responses in people exposed to cigarette smoke and how they relate to smoke-associated diseases, such as COPD, remain unclear,” said Wael Awad of Monash University. first author of the new JEM study.
The study looked at how cigarette smoke affects mucosal-associated invariant T cells (MAIT), a type of immune cell that fights infections and promotes inflammation or tissue repair. MAIT cells are activated by a protein called MR1, which detects chemicals produced by bacteria. Although the health risks of smoke are known, little is known about how its specific components affect the immune system and the body in general.
“We suspect that some of the more than 20,000 chemicals present in the cigarette smoke that smokers inhale could also bind to MR1 and influence the activity of MAIT cells in the lungs,” says Awad.
The researchers used computer modeling to identify components of cigarette smoke that interact with the MR1 protein, finding that some molecules blocked the activation of MAIT cells. Studying the effects on human and mouse cells, they found that smoke reduced the function of MAIT cells, causing the mice to have symptoms of lung disease and greater vulnerability to infections such as the flu. Prolonged exposure altered the protection provided by these cells, increasing the risk of developing COPD.
The study, the authors conclude, reveals that components of cigarette smoke can bind to the MR1 protein and reduce the functions of protective immune cells called MAIT cells. “This increases susceptibility to infections and worsens the progression of lung disease,” says Awad.
The researchers now plan to investigate exactly which MAIT cell pathways are affected by cigarette smoke, in order to learn how to better treat COPD and other lung diseases.
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