|GUPTA, ANAMIKA - University Of Arkansas|
|BASAL, MOHI - University Of Arkansas|
|WAGLE, BASANTA - University Of Arkansas|
|SUN, XIAOLUN - University Of Arkansas|
|Donoghue, Ann - Annie|
|UPADHYAY, ABHINAV - University Of Connecticut|
Submitted to: Frontiers in Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/27/2020
Publication Date: 9/16/2020
Citation: Gupta, A., Basal, M., Wagle, B., Sun, X., Rath, N.C., Donoghue, A.M., Upadhyay, A. 2020. Sodium butyrate reduces Salmonella Enteritidis infection of chicken enterocytes and expression of inflammatory host genes in-vitro. Frontiers in Microbiology. https://doi.org/10.3389/fmicb.2020.553670.
Interpretive Summary: We studied the effect of a chemical named sodium butyrate to find whether it modulates the ability of Salmonella, a bacteria that causes food poisoning, to colonize and cause sickness using intestinal cell and certain immune cells in culture. Using microbial and molecular techniques, our results show that the butyrate has the potential to prevent bacterial entry into the cells and reduce inflammation induced by infection.
Technical Abstract: Salmonella Enteritidis (SE) is a facultative intracellular pathogen, that colonizes the chicken gut in high numbers leading to contamination of carcasses during processing. A reduction in chicken intestinal colonization by SE could result in reduced carcass contamination thereby reducing the risk of enteric illnesses in humans. Hence, the objective of the present study was to determine the effect of sub-inhibitory concentrations (SICs; concentrations below minimum inhibitory concentrations that do not affect bacterial growth as compared to control) of sodium butyrate on the adhesion and invasion of SE in primary chicken enterocytes and chicken macrophages. In addition, the effect of sodium butyrate on the expression of SE virulence genes and selected inflammatory genes in chicken macrophages challenged with SE were investigated. The two SICs of sodium butyrate against SE were 22 mM and 45 mM respectively. The SICs of sodium butyrate did not affect the viability and proliferation of primary chicken enterocytes and chicken macrophage cells (P>0.05). The two SICs of sodium butyrate reduced SE adhesion by ~1.7 Log CFU/mL (98%) and ~1.8 Log CFU/mL (98.42%) respectively (P<0.05). The SE invasion was reduced by ~2 Log CFU/mL (99%) and ~2.93 Log CFU/mL (99.9%) respectively in primary chicken enterocytes (P<0.05). Sodium butyrate did not significantly affect the adhesion of SE to chicken macrophages. However, 45 mM sodium butyrate reduced invasion by ~1.7 Log CFU/mL (98%) as compared to control (P<0.05). Exposure to sodium butyrate did not change the expression of SE genes associated with motility (flgG, prot6E), invasion (invH), type 3 secretion system (sipB, pipB), survival in macrophages (spvB, mgtC), cell wall and membrane integrity (tatA), efflux pump regulator (mrr1) and global virulence regulation (lrp) (P>0.05). However, a few genes contributing to type 3 secretion system components (ssaV, sipA), adherence (sopB), macrophage survival (sodC) and oxidative stress (rpoS) were upregulated. The expression of inflammatory genes (Il1ß, Il8 and Mmp9) that are triggered by SE for host colonization was significantly downregulated by sodium butyrate as compared to control (P<0.05). The results suggest that sodium butyrate has an anti-inflammatory potential to reduce SE colonization in chickens.