University of Groningen DAMPs, endogenous danger signals fueling airway inflammation in COPD Pouwels, Simon

Therefore, it is tempting to speculate that differences in PRR expression contribute to the increased epithelial release of IL-8 and subsequent attraction of neutrophils in that

Correction for body mass index did not change the outcome of any of the GSEA analysis (data not shown). Together, these results show that cigarette smoking induces higher induction

of selected genes significantly associated with lung tissue MPO levels. H) Protein expression of IFN-α was determined in homogenized lung tissue of cigarette smoke exposed mice

We determined the DAMP signature associated with susceptibility for CS-induced neutrophilic airway inflammation by measuring the BAL levels of a selected panel of six DAMPs

In order to investigate whether the candidate genes for CS-induced dsDNA release in mice are also regulated by CS exposure in the airway epithelium in human subjects, we analyzed

Figure 1: The levels of S100A9, HMGB1 and LL37 are increased in serum of COPD patients during exacerbation. The levels of G) LL37, H) HMGB1 and I) S100A9 during exacerbation in serum

The mRNA expression of TLR2, TLR4 and NLRP3 was significantly increased in neutrophils of COPD patients during acute exacerbation compared to stable disease (Figure 1B, C, E),

To test our hypothesis that CS induces necrotic cell death in lung neutrophils, we first evaluated the direct effects of CS exposure on sputum neutrophil counts.. In an open