Abstract
Asthma is a chronic inflammatory disease, characterized by symptoms including increased mucus production, reversible airway obstruction and lung inflammation: all of which are exaggerated during asthma exacerbations. Extracellular matrix remodeling is associated with the release of ECM protein fragments (neo-epitopes) to the circulation. We sought to investigate the relationship between serological assessment of ECM remodeling markers (neo-epitopes) and the level of symptoms in a mouse model of exacerbated asthma. The hypothesis was, that an increase in ECM remodeling would be observed as a consequence of airway inflammation during exacerbations. Balb/C mice were sensitized to ovalbumin (OVA) (i.p.), acute exacerbations were provoked by i.n. instillation of poly-cytidylic-inosinic acid. Markers of matrix metalloproteinase (MMP) degraded collagen type I (C1M), type III (C3M), type IV (C4M), elastin (ELM7), and laminin (LAMa5) were assessed in serum. Analysis-software: JMP13 (SAS). Serum levels of C1M and LAMa5 individually correlated with bronchoalveolar lavage cells (BAL). Furthermore, the increase of airway resistance (C4M rs = -0.42, p <0.01; C1M, rs -0.55, p <0.001), the absolute airway resistance (C1M, rs = -0.51, p <0.001) and the dynamic compliance (C1M, rs = -0.47, p <0.01), were correlated with the ECM remodeling markers. Additionally, C1M showed a distinct correlation with the amount of mucus producing cells (Pearson coefficient 0.60, p = 0.0006). These data suggest, that serological neo-epitope markers may be valuable tools for objectively assessing the extent of airway remodeling especially during disease aggravation.
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