Abstract
Introduction. In the pathogenesis of acute respiratory distress syndrome (ARDS), signaling molecules such as cytokines play an important role in initiating, enhancing, and consolidating the inflammatory response. We aimed to identify the most indicative immunohistochemical markers for ARDS and the areas of studying them and to establish the optimal age of animals (i.e., rats) for ARDS induction. Materials and methods. We conducted a histological and immunohistochemical study of rats’ lung sections in two intact groups and two groups with a lipopolysaccharide-induced model of ARDS in three areas: bronchial epithelium, lung consolidation, and unchanged parenchyma. The rats were also divided into two age groups. We compared a microscopic appearance, the number of goblet cells, and immunohistochemical expression of IL-1β, IL-6, TNF-α, Ki-67, and CD31. Results. Both groups saw a significant increase in the number of goblet cells. At 8–10 weeks of age, the rats developed increased basal levels of IL-1β and proliferative activity in the lungs; the area of the capillary network decreased. In the experimental groups, the animals aged 4–6 weeks showed an increase in the level of IL-1β in all lung areas; however, in the animals aged 8–10 weeks, we observed this growth only in the area of unchanged parenchyma. The relative density of the capillary lung network decreased in the ARDS group aged 4–6 weeks. Conclusion. We would recommend IL-1β as an inflammatory cytokine and CD31 as endothelial marker, which reflects changes in vascular density, as immunohistochemical markers of ARDS severity on day 4 of its development. Marker changes are more stable in the 4–6-week-old animals. Keywords: IL-1b, TNF-α, Ki-67, CD31, respiratory distress syndrome, lipopolysaccharide, lung
Published Version
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