New disease mechanism in chronic smokers discovered

Published 2018-05-21 12:53. Updated 2018-05-21 12:54Denna sida på svenska
I luftvägarna hos rökare fann forskarna förhöjda nivåer av en signalsubstans som tidigare visats frisättas av immunförsvaret när vi utsätts för bakterier. Foto: iStock
I luftvägarna hos rökare fann forskarna förhöjda nivåer av en signalsubstans som tidigare visats frisättas av immunförsvaret när vi utsätts för bakterier. Foto: iStockThe researchers found high levels of an immune signalling protein in the lungs of chronic smokers. Photo: iStock 

A new study led by researchers from Karolinska Institutet shows that an immune signalling 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

The researchers found that an immune signalling protein called IL-26 (interleukin-26) is present at high levels in the lungs of these patients. 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 characterised by neutrophilic inflammation,” says Dr Karlhans Fru Che at the Institute of Environmental Medicine, Karolinska Institutet, lead author on the study.

More studies are needed

The researchers acknowledge that more studies are needed to improve the understanding of the more precise mechanisms of action of IL-26 before this cytokine can be targeted in clinical trials.

The study was carried out as a collaboration between Lund University, University of Gothenburg, University of Oulu, Karolinska University Hospital and Karolinska Institutet. The research was funded by the Swedish Heart-Lung Foundation, the Swedish Research Council, Karolinska Institutet, Region Skåne, Stockholms County Council and Region Västra Götaland, among others.

This news article is based on a press release from The Biochemical Society, which owns the journal Clinical Science.

Publication

“The neutrophil-mobilizing cytokine interleukin-26 in the airways of long-term tobacco smokers”
Karlhans Fru Che, Ellen Tufvesson, Sara Tengvall, Elisa Lappi-Blanco, Riitta Kaarteenaho, Bettina Levänen, Marie Ekberg, Annelie Brauner, Åsa M. Wheelock, Leif Bjermer, C. Magnus Sköld, Anders Lindén
Clinical Science, online 21 May 2018, doi: 10.1042/CS20180057

Chronic DiseasesCollaborationEnvironmental MedicineImmunologyPulmonary medicine