肠炎
炎症
细胞粘附分子
犬细小病毒
免疫学
细胞间粘附分子
医学
内皮细胞活化
C反应蛋白
内科学
病理
胃肠病学
生物
细小病毒
细胞粘附
细胞
病毒
遗传学
作者
B.K. Atkinson,Amelia Goddard,Monique Engelbrecht,S Pretorius,P. Pazzi
标识
DOI:10.36303/jsava.2022.93.1.496
摘要
Background: Canine parvovirus (CPV) is a common cause of enteritis, immune suppression and systemic inflammation in young dogs.Endothelial markers, such as intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and molecules that upregulate their expression, such as high mobility group box 1 protein (HMGB-1), provide insight into the state of the endothelium during inflammation.Objectives: This study aimed to determine if circulating concentrations of ICAM-1, VCAM-1 and HMGB-1 were altered in CPV enteritis compared to healthy controls, and whether a correlation existed between these molecules and the degree of inflammation.Methods: Thirty dogs with naturally occurring CPV enteritis and ten control dogs were included.Physical examinations, complete blood count and C-reactive protein (CRP) measurements were performed on all dogs at presentation.The concentrations of ICAM-1, VCAM-1 and HMGB-1 were measured using commercially available canine-specific enzyme-linked immunosorbent assay (ELISA) kits. Results:In dogs with CPV enteritis, ICAM-1 concentrations were significantly lower (median: 5.9 [IQR: 4.3-8.3])and CRP higher ) compared to controls (8.0 [IQR: 6.9-10.3],p = 0.008; 1 [IQR: 0-7], p < 0.001).No significant difference was found for VCAM-1 and HMGB-1.A strong correlation was identified between VCAM-1 and segmented neutrophil count (r = 0.612, p < 0.001). Conclusion:Despite the presence of systemic inflammation in CPV enteritis, evidenced by high CRP concentrations, our results suggest circulating concentrations of ICAM-1, VCAM-1 and HMGB-1 failed to show an increase.Endothelial activation with subsequent leukocyte adhesion and transmigration through the endothelium may be affected in CPV enteritis and these findings require further investigation.
科研通智能强力驱动
Strongly Powered by AbleSci AI