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.
Highlights
The rapid and efficient innate defense mechanisms to resist microbial invasion may contribute to the overall health and well-being of human and animals
We have previously reported that bovine neutrophils responded well for phagocytosis when supplemented with 50 μM quercetin (Chuammitri et al, 2015)
The results suggested that the expression of genes involved in that process after neutrophils has been supplemented with PBS, quercetin and Cytochalasin B (CytB) for 30 min and cells were allowed to intake opsonized bacteria for another 45 min
Summary
The rapid and efficient innate defense mechanisms to resist microbial invasion may contribute to the overall health and well-being of human and animals. Neutrophils are actively phagocytic cells performing host defense through a variety of effector functions, i.e., Reactive Oxygen Species (ROS) generation, phagocytosis, degranulation and Neutrophil Extracellular Traps (NETs) release (Amulic et al, 2012; Brinkmann et al, 2004; Chuammitri et al, 2015). Phagocytosis of human Polymorphonuclear leukocytes (PMNs) was assisted by the Fc receptor and Complement Receptors (CRs) led to the expression of many involving genes in cytokine production and signal transduction (Kobayashi et al, 2002). The available information stated that gene expression and cell signaling pathways involved in phagocytosis, AMP-activated Protein Kinase (AMPK), may result in anti-inflammatory in phagocytosis of E. coli, as well as, the changes in cytoskeletal reorganization (Bae et al, 2011). The AMPK signaling stimulated PAK1/2 genes and the RAC1 gene that helped reduce the expression of other genes
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: American Journal of Animal and Veterinary Sciences
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
