Year-end Sale % OFF 
Abstract
Salmonella enterica serovar Typhimurium infects intestinal epithelia and macrophages, which is prevented by inhibiting adhesion and cell invasion. This study aimed to investigate the role of methyl gallate (MG) in adhesion, invasion, and intracellular survival of Salmonella Typhimurium in Caco-2 and RAW 264.7 cells via a gentamicin protection assay, confocal microscopy, and quantitative reverse-transcription polymerase chain reaction. MG (30 µg/mL) inhibited adhesion and invasion of Salmonella Typhimurium by 54.01% and 60.5% in RAW 264.7 cells, respectively. The combination of MG with sub-minimum inhibitory concentration (MIC) of marbofloxacin (MRB) inhibited the adhesion, invasion, and intracellular survival by 70.49%, 67.36%, and 74%, respectively. Confocal microscopy further revealed reductions in bacterial count in Caco-2 cells treated with MG alone or with sub-MIC of MRB. Furthermore, MG alone or in combination with sub-MIC of MRB decreased the motility of Salmonella Typhimurium. Quorum sensing genes including sdiA, srgE, and rck were downregulated by 52.8%, 61.7%, and 22.2%, respectively. Moreover, rac-1 was downregulated by 56.9% and 71.9% for MG alone and combined with sub-MIC of MRB, respectively, in mammalian cells. Furthermore, MG downregulated virulence genes of Salmonella Typhimurium including cheY, ompD, sipB, lexA, and ompF by 59.6%, 60.2%, 20.5%, 31.4%, and 16.2%, respectively. Together, the present results indicate that MG alone or in combination with a sub-MIC of MRB effectively inhibited the adhesion, invasion, and intracellular survival of Salmonella Typhimurium in vitro by downregulating quorum sensing and virulence genes.
Highlights
Salmonella enterica serovar Typhimurium is a gram-negative facultative anaerobic enteric pathogen in humans and animals, and a leading cause of gastroenteritis [1]
The Salmonella pathogenicity island-1 (SPI-1) type III secretion system (T3SS) is critical for invasion of host cells via the trigger mechanism by deploying a macropinocytosisrelated process in enterocytes and the SPI-2 of the type three section system (T3SS) is responsible for the zipper mechanism and intracellular survival of Salmonella Typhimurium [7, 8]
To determine the effect of methyl gallate (MG) on nitric oxide (NO) produced by RAW 264.7 cells induced by intact Salmonella Typhimurium, Griess reagent was used
Summary
Salmonella enterica serovar Typhimurium is a gram-negative facultative anaerobic enteric pathogen in humans and animals, and a leading cause of gastroenteritis [1]. The strain invades intestinal phagocytic and epithelial (nonphagocytic) cells. Salmonella strains penetrate nonphagocytic cells via a trigger or zipper mechanism. The Salmonella pathogenicity island-1 (SPI-1) type III secretion system (T3SS) is critical for invasion of host cells via the trigger mechanism by deploying a macropinocytosisrelated process in enterocytes and the SPI-2 of the T3SS is responsible for the zipper mechanism and intracellular survival of Salmonella Typhimurium [7, 8]. Effector proteins of Salmonella SPI-1 regulate cellular invasion and enable the rearrangement of the actin cytoskeleton in the host cell. These proteins indirectly regulate the activation of the Rho GTPases including the CDC42 and Rac proteins in host cells
Sign-in/Register to view highlights & summary 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 callDisclaimer: 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.
