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Hesperidin Inhibits Inflammatory Response Induced by Aeromonas hydrophila Infection and Alters CD4(+)/CD8(+) T Cell Ratio

Background. Aeromonas hydrophila is an opportunistic bacterial pathogen that is associated with a number of human diseases. Hesperidin (HES) has been reported to exert antioxidant and anti-inflammatory activities. Objectives. The aim of this study was to investigate the potential effect of HES treat...

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Detalles Bibliográficos
Autores principales: Abuelsaad, Abdelaziz S. A., Allam, Gamal, Al-Solumani, Adnan A. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033591/
https://www.ncbi.nlm.nih.gov/pubmed/24891765
http://dx.doi.org/10.1155/2014/393217
Descripción
Sumario:Background. Aeromonas hydrophila is an opportunistic bacterial pathogen that is associated with a number of human diseases. Hesperidin (HES) has been reported to exert antioxidant and anti-inflammatory activities. Objectives. The aim of this study was to investigate the potential effect of HES treatment on inflammatory response induced by A. hydrophila infection in murine. Methods. A. hydrophila-infected mice were treated with HES at 250 mg/kg b.wt./week for 4 consecutive weeks. Phagocytosis, reactive oxygen species production, CD4(+)/CD8(+) T cell ratio, and CD14 expression on intestinal infiltrating monocytes were evaluated. The expression of E-selectin and intercellular adhesion molecule 1 on stimulated HUVECs and RAW macrophage was evaluated. Results. Percentage of CD4(+) T cells in the intestinal tissues of infected treated mice was highly significantly increased; however, phagocytic index, ROS production, CD8(+) T cells percentage, and CD14 expression on monocytes were significantly reduced. On the other hand, HES significantly inhibited A-LPS- and A-ECP-induced E-selectin and ICAM-1 expression on HUVECs and ICAM-1 expression on RAW macrophage. Conclusion. Present data indicated that HES has a potential role in the suppression of inflammatory response induced by A. hydrophila toxins through downmodulation of ROS production and CD14 and adhesion molecules expression, as well as increase of CD4(+)/CD8(+) cell ratio.