American Journal of Animal and Veterinary Sciences

Quercetin Promotes the Expression of Genes Involved in Phagocytosis in Bovine Neutrophils

Suphakit Srikok, Sukij Nambut, Kanruethai Wongsawan and Phongsakorn Chuammitri

DOI : 10.3844/ajavsp.2017.85.95

American Journal of Animal and Veterinary Sciences

Volume 12, Issue 2

Pages 85-95

Abstract

This study was conducted to explore the effect of Quercetin (QH) on phagocytosis of bovine neutrophils. Neutrophils were isolated from fifteen multiparous Holstein cows. We in vitro treated neutrophils with PBS or 50 µM of Quercetin (QH) or Cytochalasin B (CytB), as phagocytosis inhibitor, prior to monitoring phagocytosis of Escherichia coli by flow cytometry and microscopic examination. Additionally, the expressions of CORO1A, CYBA (gp91phox), LAMP1, RAB7A, RAC1 and PAK1 mRNA were analyzed by real-time PCR. In the time-course experiment, treated neutrophils were allowed to co-cultured with live bacteria for 30, 60 and 90 min before measuring gene expressions. The expression levels of IL-1 β and TNF genes in order to demonstrate the anti-inflammatory property of quercetin were assessed by conventional RT-PCR. The results of flow cytometry and microscopic examination showed that the percentage of neutrophils performing phagocytosis were significantly higher in QH group in comparison with other groups. We reported here that mRNA expressions of CORO1A, CYBA, LAMP1, RAB7A, RAC1 and PAK1 genes involved in phagocytosis, were significantly up-regulated in QH group. As expected, CytB group had profound down-regulation of genes with one exception in PAK1. From our observations, the expression levels of phagocytic process genes in the QH group were optimum at 60 min and started to decline at 90 min of incubation. The data also indicated that quercetin inhibited inflammation by reducing the expressions of both IL-1β and TNF. In conclusion, the information in our experiments conclude that quercetin has the ability to boost the expression of genes involved in phagocytosis while reduces the expression of proinflammatory genes.

Copyright

© 2017 Suphakit Srikok, Sukij Nambut, Kanruethai Wongsawan and Phongsakorn Chuammitri. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.