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SummarySalmonella typhimurium causes enteric and systemic disease by invading the intestinal epithelium of the distal ileum, a process requiring the invasion genes of Salmonella pathogenicity island 1 (SPI-1). BarA, a sensor kinase postulated to interact with the response regulator SirA, is required for the expression of SPI-1 invasion genes. We found, however, that a barA null mutation had little effect on virulence using the mouse model for septicaemia. This confounding result led us to seek environmental signals present in the distal ileum that might supplant the need for BarA. We found that acetate restored the expression of invasion genes in the barA mutant, but had no effect on a sirA mutant. Acetate had its effect only at a pH that allowed its accumulation within the bacterial cytoplasm and not with the deletion of ackA and pta , the two genes required to produce acetylphosphate. These results suggest that the rising concentration of acetate in the distal ileum provides a signal for invasion gene expression by the production of acetyl-phosphate in the bacterial cytoplasm, a pathway that bypasses barA . We also found that a D D D D ( ackA-pta ) mutation alone had no effect on virulence but, in combination with D D D D ( barA ), it increased the oral LD 50 24-fold. Thus, the combined loss of the BarA-and acetate-dependent pathways is required to reduce virulence. Two other short-chain fatty acids (SCFA), propionate and butyrate, present in high concentrations in the caecum and colon, had effects opposite to those of acetate: neither restored invasion gene expression in the barA mutant, and both, in fact, reduced expression in the wild-type strain. Further, a combination of SCFAs found in the distal ileum restored invasion gene expression in the barA mutant, whereas colonic conditions failed to do so and also reduced expression in the wild-type strain. These results suggest that the concentration and composition of SCFAs in the distal ileum provide a signal for productive infection by Salmonella , whereas those of the large intestine inhibit invasion.
SummarySalmonella typhimurium causes enteric and systemic disease by invading the intestinal epithelium of the distal ileum, a process requiring the invasion genes of Salmonella pathogenicity island 1 (SPI-1). BarA, a sensor kinase postulated to interact with the response regulator SirA, is required for the expression of SPI-1 invasion genes. We found, however, that a barA null mutation had little effect on virulence using the mouse model for septicaemia. This confounding result led us to seek environmental signals present in the distal ileum that might supplant the need for BarA. We found that acetate restored the expression of invasion genes in the barA mutant, but had no effect on a sirA mutant. Acetate had its effect only at a pH that allowed its accumulation within the bacterial cytoplasm and not with the deletion of ackA and pta , the two genes required to produce acetylphosphate. These results suggest that the rising concentration of acetate in the distal ileum provides a signal for invasion gene expression by the production of acetyl-phosphate in the bacterial cytoplasm, a pathway that bypasses barA . We also found that a D D D D ( ackA-pta ) mutation alone had no effect on virulence but, in combination with D D D D ( barA ), it increased the oral LD 50 24-fold. Thus, the combined loss of the BarA-and acetate-dependent pathways is required to reduce virulence. Two other short-chain fatty acids (SCFA), propionate and butyrate, present in high concentrations in the caecum and colon, had effects opposite to those of acetate: neither restored invasion gene expression in the barA mutant, and both, in fact, reduced expression in the wild-type strain. Further, a combination of SCFAs found in the distal ileum restored invasion gene expression in the barA mutant, whereas colonic conditions failed to do so and also reduced expression in the wild-type strain. These results suggest that the concentration and composition of SCFAs in the distal ileum provide a signal for productive infection by Salmonella , whereas those of the large intestine inhibit invasion.
Due to the rise in obesity and obesity-related conditions, there is growing commercial and public interest in foods and food components that promote health and lower risk of chronic metabolic diseases. Resistant starch (RS) is a non-viscous fermentable fiber that has beneficial metabolic effects on glucose tolerance, insulin sensitivity, and colon health in humans. While the mechanism behind the effects of RS are unclear, the benefits are thought to result from fermentation of RS in the large bowel by colonic bacteria resulting in a more favorable gut microbial composition and increased concentration of short-chain fatty acids (SCFAs). Evidence indicates that RS may result in increased colonic bacterial species Ruminococcus bromii (R. bromii), and in phylum level changes in Bacteriodetes and Fermicutes. The increase in SCFAs has been shown to potentially play a role in lowering gut pH to improve health, contribute to appetite control and reduced adipose tissue lipolysis; and reduce postprandial serum oxidative stress. Additionally, evidence indicates RS aids in treatment of diarrheal disease by interacting with both the human to increase SCFA concentration, water retention, and fecal weight and to interact with the disease-causing agent such that the insult to the human lumen cells is reduced. Therefore, RS may be a potent dietary therapy for individuals at risk for conditions including metabolic syndrome, type-2 diabetes, colorectal cancer, and diarrheal diseases. The effects of type, dose, and duration of RS intake and subsequent impact on health are important areas of further research.
The autoinducer-2 (AI-2) molecule produced by bacteria as part of quorum sensing is considered to be a universal inducer signal in bacteria because it reportedly influences gene expression in a variety of both gram-negative and gram-positive bacteria. The objective of this study was to determine whether selected fresh produce and processed foods have AI-2-like activity and whether specific food additives can act as AI-2 mimics and result in AI-2-like activity. The luminescence-based response of the reporter strain Vibrio harveyi BB170 was used as the basis for determining AI-2 activity in the selected foods and food ingredients. Maximum AI-2 activity was seen on the frozen fish sample (203-fold, compared with the negative control) followed by tomato, cantaloupe, carrots, tofu, and milk samples. Interestingly, some samples were capable of inhibiting AI-2 activity. Turkey patties showed the highest inhibition (99.8% compared with the positive control) followed by chicken breast (97.5%), homemade cheeses (93.7%), beef steak (90.6%), and beef patties (84.4%). AI-2 activity was almost totally inhibited by sodium propionate, whereas sodium benzoate caused 93.3% inhibition, compared with 75% inhibition by sodium acetate. Sodium nitrate did not have any appreciable effect, even at 200 ppm. Understanding the relationships that exist between AI-2 activity on foods and the ecology of pathogens and food spoilage bacteria on foods could yield clues about factors controlling food spoilage and pathogen virulence.
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