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Lactic acid bacteria decrease Salmonella enterica Javiana virulence and modulate host inflammation during infection of an intestinal epithelial cell line.

ABSTRACT: Salmonella enterica Javiana is a leading cause of severe foodborne Salmonellosis. Despite its emergence as a major foodborne pathogen, little is known of how S. Javiana interacts with intestinal epithelial cells, or of potential methods for ameliorating the bacterial-host interaction. Using cell-based adhesion, invasion and lactate dehydrogenase release assays, we observed an invasive and cytotoxic effect of S. Javiana on intestinal epithelial cells. We assessed the effect of probiotic species of lactic acid bacteria (LAB) on the S. Javiana-host cell interaction, and hypothesized that LAB would reduce S. Javiana infectivity. Salmonella enterica Javiana invasion was significantly impaired in host cells pre-treated with live Lactobacillus acidophilus and Lactobacillus rhamnosus. In addition, pre-exposure of host cells to live L. acidophilus, L. rhamnosus and L. casei reduced S. Javiana-induced cytotoxicity, while heat-killed LAB cultures had no effect on S. Javiana invasion or cytotoxicity. qRT-PCR analysis revealed that S. Javiana exposed to L. acidophilus and L. rhamnosus exhibited reduced virulence gene expression. Moreover, pre-treating host cells with LAB prior to S. Javiana infection reduced host cell production of inflammatory cytokines. Data suggest a potential protective effect of L. acidophilus, L. rhamnosus and L. casei against intestinal epithelial infection and pathogen-induced damage caused by S. Javiana.

SUBMITTER: Burkholder KM

PROVIDER: S-EPMC6504658 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Salmonella enterica serovar Javiana is the fourth most reported serovar of laboratory-confirmed human Salmonella infections in the U.S. and in Tennessee (TN). Although Salmonella ser. Javiana is a common cause of human infection, the majority of cases are sporadic in nature rather than outbreak-associated. To better understand Salmonella ser. Javiana microbial population structure in TN, we completed a phylogenetic analysis of 111 Salmonella ser. Javiana clinical isolates from TN collected from Jan. 2017 to Oct. 2018. We identified mobile genetic elements and genes known to confer antibiotic resistance present in the isolates, and performed a pan-genome-wide association study (pan-GWAS) to compare gene content between clades identified in this study. The population structure of TN Salmonella ser. Javiana clinical isolates consisted of three genetic clades: TN clade I (n = 54), TN clade II (n = 4), and TN clade III (n = 48). Using a 5, 10, and 25 hqSNP distance threshold for cluster identification, nine, 12, and 10 potential epidemiologically-relevant clusters were identified, respectively. The majority of genes that were found to be over-represented in specific clades were located in mobile genetic element (MGE) regions, including genes encoding integrases and phage structures (91.5%). Additionally, a large portion of the over-represented genes from TN clade II (44.9%) were located on an 87.5 kb plasmid containing genes encoding a toxin/antitoxin system (ccdAB). Additionally, we completed phylogenetic analyses of global Salmonella ser. Javiana datasets to gain a broader insight into the population structure of this serovar. We found that the global phylogeny consisted of three major clades (one of which all of the TN isolates belonged to) and two cgMLST eBurstGroups (ceBGs) and that the branch length between the two Salmonella ser. Javiana ceBGs (1,423 allelic differences) was comparable to those from other serovars that have been reported as polyphyletic (929-2,850 allelic differences). This study demonstrates the population structure of TN and global Salmonella ser. Javiana isolates, a clinically important Salmonella serovar and can provide guidance for phylogenetic cluster analyses for public health surveillance and response.

Project description:Salmonella enterica serovar Typhimurium (S. Typhimurium) is one of the leading causes of food-borne illnesses worldwide. To colonize the gastrointestinal tract, S. Typhimurium produces multiple virulence factors that facilitate cellular invasion. Chitinases have been recently emerging as virulence factors for various pathogenic bacterial species, and the S. Typhimurium genome contains two annotated chitinases: STM0018 (chiA) and STM0233. However, the role of these chitinases during S. Typhimurium pathogenesis is unknown. The putative chitinase STM0233 has not been studied previously, and only limited data exists on ChiA. Chitinases typically hydrolyze chitin polymers, which are absent in vertebrates. However, chiA expression was detected in infection models and purified ChiA cleaved carbohydrate subunits present on mammalian surface glycoproteins, indicating a role during pathogenesis. Here, we demonstrate that expression of chiA and STM0233 is upregulated in the mouse gut and that both chitinases facilitate epithelial cell adhesion and invasion. S. Typhimurium lacking both chitinases showed a 70% reduction in invasion of small intestinal epithelial cells in vitro. In a gastroenteritis mouse model, chitinase-deficient S. Typhimurium strains were also significantly attenuated in the invasion of small intestinal tissue. This reduced invasion resulted in significantly delayed S. Typhimurium dissemination to the spleen and the liver, but chitinases were not required for systemic survival. The invasion defect of the chitinase-deficient strain was rescued by the presence of wild-type S. Typhimurium, suggesting that chitinases are secreted. By analyzing N-linked glycans of small intestinal cells, we identified specific N-acetylglucosamine-containing glycans as potential extracellular targets of S. Typhimurium chitinases. This analysis also revealed a differential abundance of Lewis X/A-containing glycans that is likely a result of host cell modulation due to the detection of S. Typhimurium chitinases. Similar glycomic changes elicited by chitinase deficient strains indicate functional redundancy of the chitinases. Overall, our results demonstrate that S. Typhimurium chitinases contribute to intestinal adhesion and invasion through modulation of the host glycome.

Project description:On 10 August 2016, the Maricopa County Department of Public Health identified culture-confirmed Salmonella enterica serotype Javiana isolates from two persons who reported eating at a seafood restaurant; seven additional cases were reported by 15 August. We investigated to identify a source and prevent further illness. We interviewed persons with laboratory-reported Salmonella Javiana infection. Pulsed-field gel electrophoresis (PFGE) and whole genome sequencing of isolates were performed. A case was defined as diarrheal illness in a person during July to September 2016; confirmed cases had Salmonella Javiana isolate yielding outbreak-related PFGE patterns; probable cases had diarrheal illness and an epidemiologic link to a confirmed case. Case finding was performed (passive surveillance and identification of ill meal companions). A case-control study assessed risk factors for Salmonella Javiana infection among restaurant diners; control subjects were chosen among meal companions. No restaurant workers reported illness. Foods were reportedly cooked according to the Food Code. Food and environmental samples were collected and cultured; Salmonella Javiana with an indistinguishable PFGE pattern was isolated from portioned repackaged raw shrimp, halibut, and a freezer door handle. We identified 50 Salmonella Javiana cases (40 confirmed and 10 probable); illness onset range was from 22 July to 17 September 2016. Isolates from 40 patients had highly related PFGE patterns. Thirty-three (73%) of 45 patients interviewed reported eating at the restaurant. Among 21 case patients and 31 control subjects, unfried cooked shrimp was associated with illness (odds ratio, 6.7; 95% confidence interval, 1.8 to 24.9; P = 0.004). Among restaurant diners, laboratory and case-control evidence indicated shrimp as the possible outbreak source; poor thermal inactivation of Salmonella on shrimp is theorized as a possible cause. Cross-contamination might have prolonged this outbreak; however, the source was not identified and highlights limitations that can arise during these types of investigations.

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Lactic acid bacteria decrease Salmonella enterica Javiana virulence and modulate host inflammation during infection of an intestinal epithelial cell line.

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