oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Nutritional and Metabolic Requirements for the Infection of HeLa Cells by Salmonella enterica Serovar Typhimurium  [PDF]
Steven D. Bowden, Amanda C. Hopper-Chidlaw, Christopher J. Rice, Vinoy K. Ramachandran, David J. Kelly, Arthur Thompson
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096266
Abstract: Salmonella is the causative agent of a spectrum of human and animal diseases ranging from gastroenteritis to typhoid fever. It is a food - and water - borne pathogen and infects via ingestion followed by invasion of intestinal epithelial cells and phagocytic cells. In this study we employed a mutational approach to define the nutrients and metabolic pathways required by Salmonella enterica serovar Typhimurium during infection of a human epithelial cell line (HeLa). We deleted the key glycolytic genes, pfkA and pfkB to show that S. Typhimurium utilizes glycolysis for replication within HeLa cells; however, glycolysis was not absolutely essential for intracellular replication. Using S. Typhimurium strains deleted for genes encoding components of the phosphotransferase system and glucose transport, we show that glucose is a major substrate required for the intracellular replication of S. Typhimurium in HeLa cells. We also deleted genes encoding enzymes involved in the utilization of gluconeogenic substrates and the glyoxylate shunt and show that neither of these pathways were required for intracellular replication of S. Typhimurium within HeLa cells.
Effect of the Escherichia coli EMO strain on experimental infection by Salmonella enterica serovar Typhimurium in gnotobiotic mice
Lima-Filho, J.V.M.;Vieira, L.Q.;Arantes, R.M.E.;Nicoli, J.R.;
Brazilian Journal of Medical and Biological Research , 2004, DOI: 10.1590/S0100-879X2004000700009
Abstract: an experimental infection with salmonella enterica subsp. enterica serovar typhimurium was evaluated in gnotobiotic mice previously exposed to a plasmid-free non-pathogenic escherichia coli (emo strain). mice were exposed to emo (experimental) or not (control) 10 days before challenge with salmonella typhimurium (102 colony forming units (cfu)/mouse). survival after challenge was higher (p < 0.05) in the experimental group (16%) than in the control animals (0%). histopathological examination of the colon and ileum mucosa of the experimental group showed less extensive lesions such as edema, cell inflammatory infiltration and hyperemia. the epithelial cells of the mucosal surface and the production of the mucous layer were also better preserved in the experimental group. the population levels of salmonella typhimurium in the feces were initially 10-fold lower (p < 0.05) in the experimental groups. however, 3 days after challenge both experimental and control groups showed similar population levels ranging from 108 to 109 cfu/g of feces. the intestinal contents of total and anti-salmonella typhimurium siga were higher in the experimental groups 10 days after inoculation of e. coli emo strain. translocation of salmonella typhimurium to the spleen was 10-fold lower (p < 0.05) in the experimental group only on day 3 after infection. this was not related to an increase in the bacterial blood clearance of the animals, as shown by experimental venous challenge with e. coli b41. in conclusion, treatment of mice with e. coli emo strain promoted a relative protection against experimental infection with salmonella typhimurium. this protection was not due to the reduction of the population of pathogens in the intestine but was probably related to stimulation of the immune response.
Effect of the Escherichia coli EMO strain on experimental infection by Salmonella enterica serovar Typhimurium in gnotobiotic mice  [cached]
Lima-Filho J.V.M.,Vieira L.Q.,Arantes R.M.E.,Nicoli J.R.
Brazilian Journal of Medical and Biological Research , 2004,
Abstract: An experimental infection with Salmonella enterica subsp. enterica serovar Typhimurium was evaluated in gnotobiotic mice previously exposed to a plasmid-free non-pathogenic Escherichia coli (EMO strain). Mice were exposed to EMO (experimental) or not (control) 10 days before challenge with Salmonella Typhimurium (102 colony forming units (CFU)/mouse). Survival after challenge was higher (P < 0.05) in the experimental group (16%) than in the control animals (0%). Histopathological examination of the colon and ileum mucosa of the experimental group showed less extensive lesions such as edema, cell inflammatory infiltration and hyperemia. The epithelial cells of the mucosal surface and the production of the mucous layer were also better preserved in the experimental group. The population levels of Salmonella Typhimurium in the feces were initially 10-fold lower (P < 0.05) in the experimental groups. However, 3 days after challenge both experimental and control groups showed similar population levels ranging from 10(8) to()10(9) CFU/g of feces. The intestinal contents of total and anti-Salmonella Typhimurium sIgA were higher in the experimental groups 10 days after inoculation of E. coli EMO strain. Translocation of Salmonella Typhimurium to the spleen was 10-fold lower (P < 0.05) in the experimental group only on day 3 after infection. This was not related to an increase in the bacterial blood clearance of the animals, as shown by experimental venous challenge with E. coli B41. In conclusion, treatment of mice with E. coli EMO strain promoted a relative protection against experimental infection with Salmonella Typhimurium. This protection was not due to the reduction of the population of pathogens in the intestine but was probably related to stimulation of the immune response.
Coordinated Regulation of Virulence during Systemic Infection of Salmonella enterica Serovar Typhimurium  [PDF]
Hyunjin Yoon,Jason E. McDermott,Steffen Porwollik,Michael McClelland,Fred Heffron
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000306
Abstract: To cause a systemic infection, Salmonella must respond to many environmental cues during mouse infection and express specific subsets of genes in a temporal and spatial manner, but the regulatory pathways are poorly established. To unravel how micro-environmental signals are processed and integrated into coordinated action, we constructed in-frame non-polar deletions of 83 regulators inferred to play a role in Salmonella enteriditis Typhimurium (STM) virulence and tested them in three virulence assays (intraperitoneal [i.p.], and intragastric [i.g.] infection in BALB/c mice, and persistence in 129X1/SvJ mice). Overall, 35 regulators were identified whose absence attenuated virulence in at least one assay, and of those, 14 regulators were required for systemic mouse infection, the most stringent virulence assay. As a first step towards understanding the interplay between a pathogen and its host from a systems biology standpoint, we focused on these 14 genes. Transcriptional profiles were obtained for deletions of each of these 14 regulators grown under four different environmental conditions. These results, as well as publicly available transcriptional profiles, were analyzed using both network inference and cluster analysis algorithms. The analysis predicts a regulatory network in which all 14 regulators control the same set of genes necessary for Salmonella to cause systemic infection. We tested the regulatory model by expressing a subset of the regulators in trans and monitoring transcription of 7 known virulence factors located within Salmonella pathogenicity island 2 (SPI-2). These experiments validated the regulatory model and showed that the response regulator SsrB and the MarR type regulator, SlyA, are the terminal regulators in a cascade that integrates multiple signals. Furthermore, experiments to demonstrate epistatic relationships showed that SsrB can replace SlyA and, in some cases, SlyA can replace SsrB for expression of SPI-2 encoded virulence factors.
Oral administration of a probiotic Lactobacillus modulates cytokine production and TLR expression improving the immune response against Salmonella enterica serovar Typhimurium infection in mice
Natalia A Castillo, Gabriela Perdigón, Alejandra de Moreno de LeBlanc
BMC Microbiology , 2011, DOI: 10.1186/1471-2180-11-177
Abstract: Probiotic administration to healthy mice increased the expression of TLR2, TLR4 and TLR9 and improved the production and secretion of TNFα, IFNγ and IL-10 in the inductor sites of the gut immune response (Peyer's patches). Post infection, the continuous probiotic administration, before and after Salmonella challenge, protected the host by modulating the inflammatory response, mainly in the immune effector site of the gut, decreasing TNFα and increasing IFNγ, IL-6 and IL-10 production in the lamina propria of the small intestine.The oral administration of L. casei CRL 431 induces variations in the cytokine profile and in the TLRs expression previous and also after the challenge with S. Typhimurium. These changes show some of the immune mechanisms implicated in the protective effect of this probiotic strain against S. Typhimurium, providing an alternative way to reduce the severity of the infection.Diarrheal infections caused by bacterial enteric pathogens including Salmonella, are one of the major causes of childhood morbidity and mortality in developing countries [1]. Salmonella enterica serovar Typhimurium (S. Typhimurium) is an intracellular Gram-negative bacterium characterized by its ability to survive and replicate within eukaryotic host cells, particularly epithelial cells and macrophages. In humans, while Salmonella enterica serovar Typhi typically causes severe or sometimes lethal systemic illness called "Typhoid Fever", Salmonella Typhimurium is associated with self limiting gastroenteritis and requires treatment only in immunocompromised patients. S. Typhimurium develops in mice an infection with the same pathogenesis and clinical manifestations than S. Typhi in humans thus, this mouse model is useful for the study of this disease [2].The intestine harbours trillions of commensal bacteria that participate in digestive functions and help to protect the host from the aggression of several enteropathogens [3]. The beneficial effects of the microbiota on the h
Some putative prebiotics increase the severity of Salmonella enterica serovar Typhimurium infection in mice  [cached]
Petersen Anne,Heegaard Peter,Pedersen Anna,Andersen Jens
BMC Microbiology , 2009,
Abstract: Background Prebiotics are non-digestible food ingredients believed to beneficially affect host health by selectively stimulating the growth of the beneficial bacteria residing in the gut. Such beneficial bacteria have been reported to protect against pathogenic infections. However, contradicting results on prevention of Salmonella infections with prebiotics have been published. The aim of the present study was to examine whether S. Typhimurium SL1344 infection in mice could be prevented by administration of dietary carbohydrates with different structures and digestibility profiles. BALB/c mice were fed a diet containing 10% of either of the following carbohydrates: inulin, fructo-oligosaccharide, xylo-oligosaccharide, galacto-oligosaccharide, apple pectin, polydextrose or beta-glucan for three weeks prior to oral Salmonella challenge (107 CFU) and compared to mice fed a cornstarch-based control diet. Results The mice fed with diets containing fructo-oligosaccharide (FOS) or xylo-oligosaccharide (XOS) had significantly higher (P < 0.01 and P < 0.05) numbers of S. Typhimurium SL1344 in liver, spleen and mesenteric lymph nodes when compared to the mice fed with the cornstarch-based control diet. Significantly increased amounts (P < 0.01) of Salmonella were detected in ileal and fecal contents of mice fed with diets supplemented with apple pectin, however these mice did not show significantly higher numbers of S. Typhimyrium in liver, spleen and lymph nodes than animals from the control group (P < 0.20). The acute-phase protein haptoglobin was a good marker for translocation of S. Typhimurium in mice. In accordance with the increased counts of Salmonella in the organs, serum concentrations of haptoglobin were significantly increased in the mice fed with FOS or XOS (P < 0.001). Caecum weight was increased in the mice fed with FOS (P < 0.01), XOS (P < 0.01), or polydextrose (P < 0.001), and caecal pH was reduced in the mice fed with polydextrose (P < 0.001). In vitro fermentation in monocultures revealed that S. Typhimurium SL1344 is capable of fermenting FOS, beta-glucan and GOS with a corresponding decline in pH. Conclusion Supplementing a cornstarch-based rodent diet with 10% FOS or XOS was found to increase the translocation of S. Typhimurium SL1344 to internal organs in mice, while 10% apple pectin was found to increase the numbers of S. Typhimurium in intestinal content and feces.
Comprehensive Identification of Salmonella enterica Serovar Typhimurium Genes Required for Infection of BALB/c Mice  [PDF]
Roy R. Chaudhuri equal contributor,Sarah E. Peters equal contributor,Stephen J. Pleasance,Helen Northen,Chrissie Willers,Gavin K. Paterson,Danielle B. Cone,Andrew G. Allen,Paul J. Owen,Gil Shalom,Dov J. Stekel,Ian G. Charles ?,Duncan J. Maskell ?
PLOS Pathogens , 2009, DOI: 10.1371/journal.ppat.1000529
Abstract: Genes required for infection of mice by Salmonella Typhimurium can be identified by the interrogation of random transposon mutant libraries for mutants that cannot survive in vivo. Inactivation of such genes produces attenuated S. Typhimurium strains that have potential for use as live attenuated vaccines. A quantitative screen, Transposon Mediated Differential Hybridisation (TMDH), has been developed that identifies those members of a large library of transposon mutants that are attenuated. TMDH employs custom transposons with outward-facing T7 and SP6 promoters. Fluorescently-labelled transcripts from the promoters are hybridised to whole-genome tiling microarrays, to allow the position of the transposon insertions to be determined. Comparison of microarray data from the mutant library grown in vitro (input) with equivalent data produced after passage of the library through mice (output) enables an attenuation score to be determined for each transposon mutant. These scores are significantly correlated with bacterial counts obtained during infection of mice using mutants with individual defined deletions of the same genes. Defined deletion mutants of several novel targets identified in the TMDH screen are effective live vaccines.
Some putative prebiotics increase the severity of Salmonella enterica serovar Typhimurium infection in mice
Anne Petersen, Peter MH Heegaard, Anna L Pedersen, Jens B Andersen, Rikke B S?rensen, Hanne Fr?ki?r, Sampo J Lahtinen, Arthur C Ouwehand, Morten Poulsen, Tine R Licht
BMC Microbiology , 2009, DOI: 10.1186/1471-2180-9-245
Abstract: The mice fed with diets containing fructo-oligosaccharide (FOS) or xylo-oligosaccharide (XOS) had significantly higher (P < 0.01 and P < 0.05) numbers of S. Typhimurium SL1344 in liver, spleen and mesenteric lymph nodes when compared to the mice fed with the cornstarch-based control diet. Significantly increased amounts (P < 0.01) of Salmonella were detected in ileal and fecal contents of mice fed with diets supplemented with apple pectin, however these mice did not show significantly higher numbers of S. Typhimyrium in liver, spleen and lymph nodes than animals from the control group (P < 0.20).The acute-phase protein haptoglobin was a good marker for translocation of S. Typhimurium in mice. In accordance with the increased counts of Salmonella in the organs, serum concentrations of haptoglobin were significantly increased in the mice fed with FOS or XOS (P < 0.001). Caecum weight was increased in the mice fed with FOS (P < 0.01), XOS (P < 0.01), or polydextrose (P < 0.001), and caecal pH was reduced in the mice fed with polydextrose (P < 0.001). In vitro fermentation in monocultures revealed that S. Typhimurium SL1344 is capable of fermenting FOS, beta-glucan and GOS with a corresponding decline in pH.Supplementing a cornstarch-based rodent diet with 10% FOS or XOS was found to increase the translocation of S. Typhimurium SL1344 to internal organs in mice, while 10% apple pectin was found to increase the numbers of S. Typhimurium in intestinal content and feces.One of the basic physiological functions of the resident microbiota is that it functions as a microbial barrier against pathogens [1]. A healthy, balanced microbiota has been suggested to be predominantly saccharolytic, with significant numbers of bifidobacteria and lactobacilli [2]. The use of pre- and probiotics has thus been suggested as approaches to prevent Salmonella infections and infections by enteric pathogens in general [3-5].Prebiotics were originally defined as "non-digestible food ingredients t
Abrogation of the Twin Arginine Transport System in Salmonella enterica Serovar Typhimurium Leads to Colonization Defects during Infection  [PDF]
M. Megan Reynolds,Lydia Bogomolnaya,Jinbai Guo,Lindsay Aldrich,Danial Bokhari,Carlos A. Santiviago,Michael McClelland,Helene Andrews-Polymenis
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015800
Abstract: TatC (STM3975) is a highly conserved component of the Twin Arginine Transport (Tat) systems that is required for transport of folded proteins across the inner membrane in gram-negative bacteria. We previously identified a ΔtatC mutant as defective in competitive infections with wild type ATCC14028 during systemic infection of Salmonella-susceptible BALB/c mice. Here we confirm these results and show that the ΔtatC mutant is internalized poorly by cultured J774-A.1 mouse macrophages a phenotype that may be related to the systemic infection defect. This mutant is also defective for short-term intestinal and systemic colonization after oral infection of BALB/c mice and is shed in reduced numbers in feces from orally infected Salmonella-resistant (CBA/J) mice. We show that the ΔtatC mutant is highly sensitive to bile acids perhaps resulting in the defect in intestinal infection that we observe. Finally, the ΔtatC mutant has an unusual combination of motility phenotypes in Salmonella; it is severely defective for swimming motility but is able to swarm well. The ΔtatC mutant has a lower amount of flagellin on the bacterial surface during swimming motility but normal levels under swarming conditions.
Polyamines Are Required for Virulence in Salmonella enterica Serovar Typhimurium  [PDF]
Lotte Jelsbak, Line Elnif Thomsen, Inke Wallrodt, Peter Ruhdal Jensen, John Elmerdahl Olsen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0036149
Abstract: Sensing and responding to environmental cues is a fundamental characteristic of bacterial physiology and virulence. Here we identify polyamines as novel environmental signals essential for virulence of Salmonella enterica serovar Typhimurium, a major intracellular pathogen and a model organism for studying typhoid fever. Central to its virulence are two major virulence loci Salmonella Pathogenicity Island 1 and 2 (SPI1 and SPI2). SPI1 promotes invasion of epithelial cells, whereas SPI2 enables S. Typhimurium to survive and proliferate within specialized compartments inside host cells. In this study, we show that an S. Typhimurium polyamine mutant is defective for invasion, intracellular survival, killing of the nematode Caenorhabditis elegans and systemic infection of the mouse model of typhoid fever. Virulence of the mutant could be restored by genetic complementation, and invasion and intracellular survival could, as well, be complemented by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection. Interestingly, intracellular survival of the polyamine mutant was significantly enhanced above the wild type level by the addition of exogenous putrescine and spermidine to the bacterial cultures prior to infection, indicating that these polyamines function as an environmental signal that primes S. Typhimurium for intracellular survival. Accordingly, experiments addressed at elucidating the roles of these polyamines in infection revealed that expression of genes from both of the major virulence loci SPI1 and SPI2 responded to exogenous polyamines and was reduced in the polyamine mutant. Together our data demonstrate that putrescine and spermidine play a critical role in controlling virulence in S. Typhimurium most likely through stimulation of expression of essential virulence loci. Moreover, our data implicate these polyamines as key signals in S. Typhimurium virulence.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.