A new study led by researchers from Karolinska Institutet shows that an immune signaling protein called IL-26 is increased among chronic smokers with lung disease. This involvement reveals disease mechanisms of interest for developing more effective therapy for these hard-to-treat patients. The study is published in the journal Clinical Science.

Chronic tobacco smokers have an increased rate of chronic obstructive pulmonary disease (COPD), chronic bronchitis, and bacterial lung infections and these disorders respond poorly to available therapies. Previous research has shown that smokers with lung disease have an accumulation of a type of white blood cell, called neutrophils, in their airways. Dr. Karlhans Fru Che and Professor Anders Lindén at Karolinska Institutet led a team of researchers from universities in Sweden and Finland to investigate why this is the case.

May represent a novel mechanism

IL-26 levels were higher than normal in the chronic smokers, regardless of whether they had clinically stable COPD. Those who had chronic bronchitis or growth of bacteria had higher levels of IL-26 than those who did not. Moreover, the chronic smokers with exacerbations of COPD had higher levels of IL-26 than those with clinically stable COPD. Upregulation of IL-26 in the airways in response to tobacco smoke may represent a novel mechanism by which neutrophil recruitment to the lung is regulated, according to the researchers.

“By showing that IL-26 is involved in the excessive mobilization of neutrophils in chronic smokers with or without COPD and chronic bronchitis, we strengthen the evidence that this cytokine bears potential as a target for monitoring of and therapeutic intervention in airway disorders characterized by neutrophilic inflammation,” says Dr. Karlhans Fru Che at the Institute of Environmental Medicine, Karolinska Institutet, lead author on the study.