Abstract
BackgroundResults from preclinical studies suggest that age-dependent differences in host defense and the pulmonary renin–angiotensin system (RAS) are responsible for observed differences in epidemiology of acute respiratory distress syndrome (ARDS) between children and adults. The present study compares biomarkers of host defense and RAS in bronchoalveolar lavage (BAL) fluid from neonates, children, adults, and older adults with ARDS.MethodsIn this prospective observational study, we enrolled mechanical ventilated ARDS patients categorized into four age groups: 20 neonates (< 28 days corrected postnatal age), 29 children (28 days–18 years), 26 adults (18–65 years), and 17 older adults (> 65 years of age). All patients underwent a nondirected BAL within 72 h after intubation. Activities of the two main enzymes of RAS, angiotensin converting enzyme (ACE) and ACE2, and levels of biomarkers of inflammation, endothelial activation, and epithelial damage were determined in BAL fluid.ResultsLevels of myeloperoxidase, interleukin (IL)-6, IL-10, and p-selectin were higher with increasing age, whereas intercellular adhesion molecule-1 was higher in neonates. No differences in activity of ACE and ACE2 were seen between the four age groups.ConclusionsAge-dependent differences in the levels of biomarkers in lungs of ARDS patients are present. Especially, higher levels of markers involved in the neutrophil response were found with increasing age. In contrast to preclinical studies, age is not associated with changes in the pulmonary RAS.
Highlights
Results from preclinical studies suggest that age-dependent differences in host defense and the pul‐ monary renin–angiotensin system (RAS) are responsible for observed differences in epidemiology of acute respiratory distress syndrome (ARDS) between children and adults
Maturation and aging-induced changes in biological pathways involved in the host response to injurious pulmonary and non-pulmonary insults may in part account for observed differences in prevalence and outcome of acute respiratory distress syndrome (ARDS) among
In all four age groups, ARDS was considered to have a direct cause in most cases
Summary
Results from preclinical studies suggest that age-dependent differences in host defense and the pul‐ monary renin–angiotensin system (RAS) are responsible for observed differences in epidemiology of acute respiratory distress syndrome (ARDS) between children and adults. The present study compares biomarkers of host defense and RAS in bronchoalveolar lavage (BAL) fluid from neonates, children, adults, and older adults with ARDS. Maturation and aging-induced changes in biological pathways involved in the host response to injurious pulmonary and non-pulmonary insults may in part account for observed differences in prevalence and outcome of acute respiratory distress syndrome (ARDS) among. We investigated biomarkers of inflammation, endothelial activation, epithelial damage, and enzymatic activities of the pulmonary RAS in bronchoalveolar lavage (BAL) fluid collected from ARDS patients at different ages. We hypothesized that aging is associated with an intensified host response and a shift in the balance from ACE2 to ACE in ARDS
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