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Researchers at Karolinska Institutet in Sweden report that a recently discovered inflammatory mediator, interleukin-26, appears to have an important role in pneumonia and contribute to the killing of bacteria. The study is published in the scientific journal Frontiers in Immunology — Microbial Immunology.
Bacterial lung infection affects both children and adults worldwide and pneumonia remains a common cause of premature death in many parts of the world, with millions of people dying from it every year. To facilitate the development of more effective therapies, researchers at Karolinska Institutet are trying to characterise the immunological mechanisms involved in pneumonia.
The new study demonstrates that an inflammatory mediator called interleukin-26 (IL-26) is critically involved in bacterial pneumonia in humans. During the last decade, IL-26 has emerged as an important player in the so-called innate immune response, our first line of defence against pathogens. It is abundant in the airways of healthy humans, and bacterial exposure stimulates an increased release of IL-26 by lung cells and white blood cells.
Studying human lung tissue and airway samples from patients with bacterial pneumonia, the researchers were able to show that IL-26 exerts complex modulatory effects on the immune system and that the protein directly kills bacteria known to cause pneumonia.
“Antibiotics are not sufficient to treat pneumonia and antibiotic resistance is an increasing problem, highlighting the need for biological treatments of this global killer disease. Our findings position IL-26 as a new potential target for biological treatment and emphasise that its role in pneumonia deserves to be further evaluated,” says lead author Karlhans Che, a researcher at the Institute of Environmental Medicine, Karolinska Institutet.
The research was financed by the Swedish Heart-Lung Foundation, The Swedish Research Council, Region Stockholm (ALF funding), and The Swedish Society for Medical Research.
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