Abstract
Do we need biomarkers of lung damage and infection: For what purpose and how should they be used properly? Biomarkers of lung damage can be used for diagnosis, risk stratification/prediction, treatment surveillance and adjustment of targeted therapy. Additionally, novel “omics” methods may offer a completely different and effective way of improving the understanding of pathogenesis of lung damage and a way to develop new candidate lung damage biomarkers. In the current review, we give an overview within the field of acute lung damage of (i) disease mechanism biomarkers, (ii) of “ready to use” evidence-based biomarker-guided lung infection management, (iii) of novel strategies of inflammatory phenotyping and how this can be used to tailor corticosteroid treatment, (iv) a future perspective of where “omics” technologies and mindsets may become increasingly important in developing new strategies for treatment and for understanding the development of acute lung damage.
Highlights
Acute lung injury is characterized by hypoxemia, bilateral opacities on chest imaging like chest X-ray or CT-scans and the condition should not be fully explained by cardiac failure or fluid overload
Since a comprehensive review of all biomarkers of lung injury would not fit into a single article, we focus on the following areas where biomarkers may be of special importance, and in which specific biomarkers have already been thoroughly investigated: (i) biomarkers of alveolar and bronchiolar damage, (ii) biomarkers of endothelial damage, (iii) biomarkers of lung infection, (iv) biomarkers to characterize phenotypic lung inflammation
COPD patients with lower blood eosinophil count have shown to be associated with increased risk of pneumonia, irrespective of ICS use [38], and these patients may not benefit from systemic corticosteroid treatment [36]
Summary
There are few biomarkers of injury involving the bronchi and bronchioles. Plasma concentration of club cell secretory protein 16 (CC16) increases due to increased permeability of the air–blood barrier within the conductive airways where the club (or clara) cells responsible for CC16 production are located [12]. CC16 will not be described in further detail in this review
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