DAMPs activating innate and adaptive immune responses in COPDPouwels, S. D., Heijink, I. H., ten Hacken, N. H. T., Vandenabeele, P., Krysko, D. V., Nawijn, M. C. & van Oosterhout, A. J. M., Mar-2014, In : Mucosal immunology. 7, 2, p. 215-226 12 p.
Research output: Contribution to journal › Review article › Academic › peer-review
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.
|Number of pages||12|
|Publication status||Published - Mar-2014|
- OBSTRUCTIVE PULMONARY-DISEASE, ENDOPLASMIC-RETICULUM STRESS, GLYCATION END-PRODUCTS, PROTEIN-COUPLED RECEPTORS, FORMYL-PEPTIDE RECEPTORS, ENDOTHELIAL-CELL DEATH, CIGARETTE-SMOKE, ANTIMICROBIAL PEPTIDES, BRONCHOALVEOLAR LAVAGE, HUMAN MONOCYTES