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Objective: To investigate the effect of respiratory syncytial virus (RSV)-related pulmonary infection on endogenous metabolites in large intestinal mucosa in BALB/c mice using metabolomics technology based on gas chromatography-mass spectrometry (GC-MS)., Methods: Mice were randomly divided into a control group and a RSV pneumonia model group (n=16 each). The mouse model of RSV pneumonia was established using intranasal RSV infection (100×TCID 50 , 50 μL/mouse, once a day). After 7 days of intranasal RSV infection, the mice were sacrificed and GC-MS was used to identify endogenous metabolites and measure the changes in their relative content in colon tissue. SMCA-P12.0 software was used to perform principal component analysis (PCA) and orthogonal partial least squares-discriminant analysis (OPLS-DA) for endogenous metabolites in colon tissue. The differentially expressed metabolites in colon tissue were imported into the metabolic pathway platform Metaboanalyst to analyze related metabolic pathways., Results: PCA and OPLS-DA showed significant differences between the control and RSV pneumonia model groups. A total of 32 metabolites were identified in the colon tissue of the mice with RSV pneumonia. The RSV pneumonia model group had significant increases in the content of leucine, isoleucine, glycine, alanine, arachidonic acid, and lactic acid, which were related to the valine, leucine, isoleucine, arachidonic acid, and pyruvic acid metabolic pathways., Conclusions: RSV pneumonia might cause metabolic disorders in the large intestinal tissue in mice.

Objective: To explore the effects of respiratory syncytial virus (RSV) upon the expressions of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1) in human embryonic lung fibroblast cells., Methods: The expressions of mRNA and protein of ICAM-1 were determined in human embryonic lung fibroblast cells after being infected by the LONG strain type A RSV and in normal fibroblast cells with real-time PCR and flow cytometry., Results: The mRNA of ICAM-1 expression in human embryonic lung fibroblast cells was 2.51 times at 24 h post-infection as that in normal fibroblast cells (P < 0.05). The protein of ICAM-1 expression of RSV control group (1.25 +/- 0.09, 1.87 +/- 0.18, 4.78 +/- 0.52, 13.34 +/- 0.64, 1.58 +/- 0.37) were significantly higher than those of normal cell group (0.21 +/- 0.06, 0.30 +/- 0.06, 0.29 +/- 0.07, 0.35 +/- 0.17, 0.35 +/- 0.14) at 12, 24, 48, 72 and 96 h post-infection (all P < 0.01). The protein of ICAM-1 expression of RSV control group achieved a peak value between 48 h and 72 h, and then it decreased significantly at 96 h., Conclusion: Lung fibroblast cell and ICAM-1 may play some roles in pathogenic mechanism of RSV viral pneumonia.