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Immunological pathways in virus-induced COPD exacerbations: a role for IL-15
Mihnea T Zdrenghea1, Patrick Mallia, Sebastian L Johnston
1Oncology Institute Prof. Dr. Ion Chiricuta, Department of Hematology and University of Medicine and Pharmacy Cluj-Napoca, Romania. mzdrenghea@umfcluj.ro
European Journal of Clinical Investigation
|April 11, 2012
Summary
Interleukin-15 (IL-15) may drive airway inflammation in chronic obstructive pulmonary disease (COPD) by boosting type 1 immune responses and affecting cytotoxic cells during virus infections.
Area of Science:
- Immunology
- Respiratory Medicine
- Molecular Biology
Background:
- Chronic obstructive pulmonary disease (COPD) features elevated type 1 interferon-γ and CD8(+) T cells.
- COPD exacerbations, often triggered by respiratory viruses and bacterial colonization, significantly increase morbidity and mortality.
- Latent viral infections may contribute to chronic inflammation in stable COPD.
Purpose of the Study:
- To review the role of interleukin-15 (IL-15) and MHC class I-related molecules (MIC A/B) in type 1 immune responses to respiratory viruses.
- To investigate the potential involvement of IL-15 in virus-induced COPD exacerbations.
Main Methods:
- Literature review on IL-15 and MIC A/B in type 1 immunity and respiratory virus infections.
- Presentation of original data suggesting IL-15's role in virus-induced COPD exacerbations.
Main Results:
- Resident airway cells (epithelial cells, macrophages) produce IL-15 in response to viral and bacterial infections.
- Respiratory viral infections alter the expression of MIC A/B molecules on respiratory epithelial cells.
Conclusions:
- IL-15 may directly contribute to COPD airway inflammation by enhancing type 1 immunity and reducing apoptosis.
- IL-15 might indirectly influence COPD inflammation by modulating MIC A/B, affecting natural killer and CD8(+) T cell cytotoxicity.
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