Co-infection by Salmonella enterica subsp. Enterica serovar typhimurium and Entamoeba dispar pathogenic strains enhances colitis and the expression of amoebic virulence factors

2021 ◽  
pp. 105010
Author(s):  
Fabrício Marcus Silva Oliveira ◽  
Ana Claúdia de Carvalho Fernandes ◽  
Sávio Henrique de Cicco Sandes ◽  
Luana Oliveira Prata ◽  
Mario Abatemarco Junior ◽  
...  
Keyword(s):  
Virulence Factors ◽  
Salmonella Enterica ◽  
Entamoeba Dispar ◽  
Serovar Typhimurium

scholarly journals Flagella and Chemotaxis Are Required for Efficient Induction of Salmonella enterica Serovar Typhimurium Colitis in Streptomycin-Pretreated Mice

2004 ◽  
Vol 72 (7) ◽  
pp. 4138-4150 ◽  
Author(s):  
Bärbel Stecher ◽  
Siegfried Hapfelmeier ◽  
Catherine Müller ◽  
Marcus Kremer ◽  
Thomas Stallmach ◽  
...  
Keyword(s):  
Virulence Factors ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Innate Immune ◽  
Gastrointestinal Infections ◽  
Infection Models ◽  
Serovar Typhimurium ◽  
Efficient Induction ◽  
Toll Like Receptor 5

ABSTRACT Salmonella enterica subspecies 1 serovar Typhimurium is a common cause of gastrointestinal infections. The host's innate immune system and a complex set of Salmonella virulence factors are thought to contribute to enteric disease. The serovar Typhimurium virulence factors have been studied extensively by using tissue culture assays, and bovine infection models have been used to verify the role of these factors in enterocolitis. Streptomycin-pretreated mice provide an alternative animal model to study enteric salmonellosis. In this model, the Salmonella pathogenicity island 1 type III secretion system has a key virulence function. Nothing is known about the role of other virulence factors. We investigated the role of flagella in murine serovar Typhimurium colitis. A nonflagellated serovar Typhimurium mutant (fliGHI) efficiently colonized the intestine but caused little colitis during the early phase of infection (10 and 24 h postinfection). In competition assays with differentially labeled strains, the fliGHI mutant had a reduced capacity to get near the intestinal epithelium, as determined by fluorescence microscopy. A flagellated but nonchemotactic cheY mutant had the same virulence defects as the fliGHI mutant for causing colitis. In competitive infections, both mutants colonized the intestine of streptomycin-pretreated mice by day 1 postinfection but were outcompeted by the wild-type strain by day 3 postinfection. Together, these data demonstrate that flagella are required for efficient colonization and induction of colitis in streptomycin-pretreated mice. This effect is mostly attributable to chemotaxis. Recognition of flagellar subunits (i.e., flagellin) by innate immune receptors (i.e., Toll-like receptor 5) may be less important.

scholarly journals Salmonella enterica serovar Typhimurium chitinases modulate the intestinal glycome and promote small intestinal invasion

2021 ◽  
Author(s):  
Jason R Devlin ◽  
William Santus ◽  
Jorge Mendez ◽  
Wenjing Peng ◽  
Aiying Yu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Virulence Factors ◽  
Salmonella Enterica ◽  
Intestinal Epithelial Cells ◽  
Bacterial Species ◽  
Intestinal Epithelial ◽  
Food Borne ◽  
Serovar Typhimurium ◽  
Small Intestinal ◽  
Adhesion And Invasion

AbstractSalmonella enterica serovar Typhimurium (Salmonella) is one of the leading causes of food-borne illnesses worldwide. To colonize the gastrointestinal tract, Salmonella produces multiple virulence factors that facilitate cellular invasion. Chitinases have been recently emerging as virulence factors for various pathogenic bacterial species and the Salmonella genome contains two annotated chitinases: STM0018 (chiA) and STM0233. However, the role of these chitinases during Salmonella 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. Salmonella lacking both chitinases showed a 70% reduction in invasion of small intestinal epithelial cells in vitro. In a gastroenteritis mouse model, chitinase-deficient Salmonella strains were also significantly attenuated in the invasion of small intestinal tissue. This reduced invasion resulted in significantly delayed Salmonella 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 Salmonella, 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 Salmonella chitinases. This analysis also revealed differential abundance of Lewis X-containing glycans that is likely a result of host cell modulation due to the detection of Salmonella chitinases. Similar glycomic changes elicited by chitinase deficient strains indicate functional redundancy of the chitinases. Overall, our results demonstrate that Salmonella chitinases contribute to intestinal adhesion and invasion through modulation of the host glycome.Author SummarySalmonella Typhimurium infection is one of the leading causes of food-borne illnesses worldwide. In order for Salmonella to effectively cause disease, it has to invade the epithelial cells lining the intestinal tract. This invasion step allows Salmonella to replicate efficiently, causing further tissue damage and inflammation. In susceptible patients, Salmonella can spread past the intestines and infect peripheral organs. It is essential to fully understand the invasion mechanism used by Salmonella to design better treatments for infection. Here, we demonstrate that the two chitinases produced by Salmonella are involved in this invasion process. We show that Salmonella chitinases interact with surface glycans of intestinal epithelial cells and promote adhesion and invasion. Using a mouse infection model, we show that Salmonella chitinases are required for the invasion of the small intestine and enhance the dissemination of Salmonella to other organs. This study reveals an additional mechanism by which Salmonella invades and causes infection.

scholarly journals Genome sequencing and analysis ofSalmonella entericasubsp.entericaserovar Stanley UPM 517: Insights on its virulence-associated elements and their potentials as vaccine candidates

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6948
Author(s):  
Khalidah Syahirah Ashari ◽  
Najwa Syahirah Roslan ◽  
Abdul Rahman Omar ◽  
Mohd Hair Bejo ◽  
Aini Ideris ◽  
...  
Keyword(s):  
Genome Sequencing ◽  
Virulence Factors ◽  
Salmonella Enterica ◽  
Draft Genome ◽  
Genomic Analysis ◽  
Farm Animals ◽  
Pathogenicity Islands ◽  
Type I ◽  
Serovar Typhimurium ◽  
Restriction Modification

Salmonella entericasubsp.entericaserovar Stanley (S. Stanley) is a pathogen that contaminates food, and is related toSalmonellaoutbreaks in a variety of hosts such as humans and farm animals through products like dairy items and vegetables. Despite the fact that several vaccines ofSalmonellastrains had been constructed, none of them were developed according to serovar Stanley up to this day. This study presents results of genome sequencing and analysis on ourS. Stanley UPM 517 strain taken from fecal swabs of 21-day-old healthy commercial chickens in Perak, Malaysia and usedSalmonella entericasubsp.entericaserovar Typhimurium LT2 (S. Typhimurium LT2) as a reference to be compared with. First, sequencing and assembling of theSalmonellaStanley UPM 517 genome into a contiguous form were done. The work was then continued with scaffolding and gap filling. Annotation and alignment of the draft genome was performed withS. Typhimurium LT2. The other elements of virulence estimated in this study includedSalmonellapathogenicity islands, resistance genes, prophages, virulence factors, plasmid regions, restriction-modification sites and the CRISPR-Cas system. TheS. Stanley UPM 517 draft genome had a length of 4,736,817 bp with 4,730 coding sequence and 58 RNAs. It was discovered via genomic analysis on this strain that there were antimicrobial resistance properties toward a wide variety of antibiotics. Tcf and ste, the two fimbrial virulence clusters related with human and broiler intestinal colonizations which were not found inS. Typhimurium LT2, were atypically discovered in theS. Stanley UPM 517 genome. These clusters are involved in the intestinal colonization of human and broilers, respectively. There were sevenSalmonellapathogenicity islands (SPIs) within the draft genome, which contained the virulence factors associated withSalmonellainfection (except SPI-14). Five intact prophage regions, mostly comprising of the protein encoding Gifsy-1, Fels-1, RE-2010 and SEN34 prophages, were also encoded in the draft genome. Also identified were Type I–III restriction-modification sites and the CRISPR-Cas system of the Type I–E subtype. As this strain exhibited resistance toward numerous antibiotics, we distinguished several genes that had the potential for removal in the construction of a possible vaccine candidate to restrain and lessen the pervasiveness of salmonellosis and to function as an alternative to antibiotics.

scholarly journals In Vivo Genetic Analysis Indicates That PhoP-PhoQ and the Salmonella Pathogenicity Island 2 Type III Secretion System Contribute Independently to Salmonella enterica Serovar Typhimurium Virulence

2001 ◽  
Vol 69 (12) ◽  
pp. 7254-7261 ◽  
Author(s):  
Carmen R. Beuzón ◽  
Kate E. Unsworth ◽  
David W. Holden
Keyword(s):  
Virulence Factors ◽  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Type Iii Secretion System ◽  
Pathogenicity Island ◽  
Secretion System ◽  
Type Iii ◽  
Serovar Typhimurium

ABSTRACT Many virulence factors are required for Salmonella enterica serovar Typhimurium to replicate intracellularly and proliferate systemically within mice. In this work, we have carried out genetic analyses in vivo to determine the functional relationship between two major virulence factors necessary for systemic infection byS. enterica serovar Typhimurium: theSalmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS) and the PhoP-PhoQ two-component regulatory system. Although previous work suggested that PhoP-PhoQ regulates SPI-2 TTSS gene expression in vitro, in vivo competitive analysis of mutant strains indicates that these systems contribute independently toS. typhimurium virulence. Our results also suggest that mutation of phoP may compensate partially for defects in the SPI-2 TTSS by deregulating SPI-1 TTSS expression. These results provide an explanation for previous reports showing an apparent functional overlap between these two systems in vitro.

scholarly journals Characterization of grvA, an Antivirulence Gene on the Gifsy-2 Phage in Salmonella enterica Serovar Typhimurium

2001 ◽  
Vol 183 (2) ◽  
pp. 611-620 ◽  
Author(s):  
Theresa D. Ho ◽  
James M. Slauch
Keyword(s):  
Virulence Factors ◽  
Salmonella Enterica ◽  
Single Copy ◽  
Null Mutation ◽  
Multicopy Plasmid ◽  
Wild Type ◽  
Reading Frame ◽  
Serovar Typhimurium ◽  
Phage Production ◽  
Superoxide Dismutase Gene

ABSTRACT The lambdoid phage Gifsy-2 contributes significantly toSalmonella enterica serovar Typhimurium virulence. The phage carries the periplasmic superoxide dismutase gene,sodCI, and other unidentified virulence factors. We have characterized the gene grvA, a single open reading frame inserted in the opposite orientation in the tail operon of the Gifsy-2 phage. Contrary to what is observed with classic virulence genes,grvA null mutants were more virulent than wild type as measured by intraperitoneal competition assays in mice. We have termed this effect antivirulence. Wild-type grvA in single copy complemented this phenotype. However, grvA +on a multicopy plasmid also conferred the antivirulence phenotype. Neither a grvA null mutation nor thegrvA + plasmid conferred a growth advantage or disadvantage in laboratory media. The antivirulence phenotype conferred by the grvA null mutation and thegrvA + plasmid required wild-typesodCI but was independent of other virulence factors encoded on Gifsy-2. These results suggest that in a wild-type situation, GrvA decreases the pathogenicity of serovar Typhimurium in the host, most likely by affecting resistance to toxic oxygen species. These virulence phenotypes were independent of functional Gifsy-2 phage production. Our data suggest that the contribution of Gifsy-2 is a complicated sum of both positive virulence factors such assodCI and antivirulence factors such asgrvA.

scholarly journals Identification and Characterization of Outer Membrane Vesicle-Associated Proteins in Salmonella enterica Serovar Typhimurium

2014 ◽  
Vol 82 (10) ◽  
pp. 4001-4010 ◽  
Author(s):  
Jaewoo Bai ◽  
Seul I Kim ◽  
Sangryeol Ryu ◽  
Hyunjin Yoon
Keyword(s):  
Outer Membrane ◽  
Virulence Factors ◽  
Salmonella Enterica ◽  
Minimal Medium ◽  
Environmental Changes ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Content Type ◽  
Serovar Typhimurium ◽  
Associated Proteins

ABSTRACTSalmonella entericaserovar Typhimurium is a primary cause of enteric diseases and has acquired a variety of virulence factors during its evolution into a pathogen. Secreted virulence factors interact with commensal flora and host cells and enableSalmonellato survive and thrive in hostile environments. Outer membrane vesicles (OMVs) released from many Gram-negative bacteria function as a mechanism for the secretion of complex mixtures, including virulence factors. We performed a proteomic analysis of OMVs that were isolated under standard laboratory and acidic minimal medium conditions and identified 14 OMV-associated proteins that were observed in the OMV fraction isolated only under the acidic minimal medium conditions, which reproduced the nutrient-deficient intracellular milieu. The inferred roles of these 14 proteins were diverse, including transporter, enzyme, and transcriptional regulator. The absence of these proteins influencedSalmonellasurvival inside murine macrophages. Eleven of these proteins were predicted to possess secretion signal sequences at their N termini, and three (HupA, GlnH, and PhoN) of the proteins were found to be translocated into the cytoplasm of host cells. The comparative proteomic profiling of OMVs performed in this study revealed different protein compositions in the OMVs isolated under the two different conditions, which indicates that the OMV cargo depends on the growth conditions and provides a deeper insight into howSalmonellautilizes OMVs to adapt to environmental changes.

scholarly journals The SopEΦ Phage Integrates into the ssrA Gene of Salmonella enterica Serovar Typhimurium A36 and Is Closely Related to the Fels-2 Prophage

2003 ◽  
Vol 185 (17) ◽  
pp. 5182-5191 ◽  
Author(s):  
Cosima Pelludat ◽  
Susanne Mirold ◽  
Wolf-Dietrich Hardt
Keyword(s):  
Virulence Factors ◽  
Virulence Factor ◽  
Salmonella Enterica ◽  
Defense Mechanisms ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Attachment Site ◽  
Host Cells ◽  
Gram Negative Bacteria ◽  
Large Array ◽  
Serovar Typhimurium

ABSTRACT Salmonella spp. are enteropathogenic gram-negative bacteria that use a large array of virulence factors to colonize the host, manipulate host cells, and resist the host's defense mechanisms. Even closely related Salmonella strains have different repertoires of virulence factors. Bacteriophages contribute substantially to this diversity. There is increasing evidence that the reassortment of virulence factor repertoires by converting phages like the GIFSY phages and SopEΦ may represent an important mechanism in the adaptation of Salmonella spp. to specific hosts and to the emergence of new epidemic strains. Here, we have analyzed in more detail SopEΦ, a P2-like phage from Salmonella enterica serovar Typhimurium DT204 that encodes the virulence factor SopE. We have cloned and characterized the attachment site (att) of SopEΦ and found that its 47-bp core sequence overlaps the 3′ terminus of the ssrA gene of serovar Typhimurium. Furthermore, we have demonstrated integration of SopEΦ into the cloned attB site of serovar Typhimurium A36. Sequence analysis of the plasmid-borne prophage revealed that SopEΦ is closely related to (60 to 100% identity over 80% of the genome) but clearly distinct from the Fels-2 prophage of serovar Typhimurium LT2 and from P2-like phages in the serovar Typhi CT18 genome. Our results demonstrate that there is considerable variation among the P2-like phages present in closely related Salmonella spp.

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