DAMPs activating innate and adaptive immune responses in COPD |
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| Affiliation: | 1. Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands;2. GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands;3. Department of Pulmonary Disease, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands;4. Department for Molecular Biomedical Research, Molecular Signaling and Cell Death Unit, VIB, Ghent, Belgium;5. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium |
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| Abstract: | Chronic obstructive pulmonary disease (COPD), a progressive lung disease characterized by sustained neutrophilic airway inflammation, is caused by chronic exposure to noxious stimuli, e.g., cigarette smoke. This chronic exposure can induce immunogenic cell death of structural airway cells, inducing the release of damage-associated molecular patterns (DAMPs). Levels of several DAMPs, including S100 proteins, defensins, and high-mobility group box-1 (HMGB1), are increased in extracellular lung fluids of COPD patients. As DAMPs can attract and activate immune cells upon binding to pattern recognition receptors, we propose that their release may contribute to neutrophilic airway inflammation. In this review, we discuss the novel role of DAMPs in COPD pathogenesis. Relevant DAMPs are categorized based on their subcellular origin, i.e. cytoplasm, endoplasmic reticulum, nucleus, and mitochondria. Furthermore, their potential role in the pathophysiology of COPD will be discussed. |
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