scholarly journals Role of the virulence plasmid in acid resistance of Shigella flexneri

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chang Niu ◽  
Jing Yang ◽  
Hongsheng Liu ◽  
Yong Cui ◽  
Huijie Xu ◽  
...  
Keyword(s):  
Shigella Flexneri ◽  
Acid Resistance ◽  
Virulence Plasmid

scholarly journals Characterization of SlyA in Shigella flexneri Identifies a Novel Role in Virulence

2016 ◽  
Vol 84 (4) ◽  
pp. 1073-1082 ◽  
Author(s):  
Natasha Weatherspoon-Griffin ◽  
Helen J. Wing
Keyword(s):  
Response Regulator ◽  
Shigella Flexneri ◽  
Acid Resistance ◽  
Enteric Bacteria ◽  
Content Type ◽  
Related Organism ◽  
Serovar Typhimurium ◽  
Exogenous Expression

The SlyA transcriptional regulator has important roles in the virulence and pathogenesis of several members of theEnterobacteriaceaefamily, includingSalmonella entericaserovar Typhimurium andEscherichia coli. Despite the identification of theslyAgene inShigella flexnerinearly 2 decades ago, as well as the significant conservation of SlyA among enteric bacteria, the role of SlyA inShigellaremains unknown. The genes regulated by SlyA in closely related organisms often are absent from or mutated inS. flexneri, and consequently many described SlyA-dependent phenotypes are not present. By characterizing the expression ofslyAand determining its ultimate effect in this highly virulent organism, we postulated that novel SlyA-regulated virulence phenotypes would be identified. In this study, we report the first analysis of SlyA inShigellaand show that (i) theslyAgene is transcribed and ultimately translated into protein, (ii)slyApromoter activity is maximal during stationary phase and is negatively autoregulated and positively regulated by the PhoP response regulator, (iii) the exogenous expression ofslyArescues transcription and virulence-associated deficiencies during virulence-repressed conditions, and (iv) the absence ofslyAsignificantly decreases acid resistance, demonstrating a novel and important role inShigellavirulence. Cumulatively, our study illustrates unexpected parallels between the less conservedS. flexneriandS. TyphimuriumslyApromoters as well as a unique role for SlyA inShigellavirulence that has not been described previously in any closely related organism.

scholarly journals Genetic Mechanisms behind the Spread of Reduced Susceptibility to Azithromycin in Shigella Strains Isolated from Men Who Have Sex with Men in Québec, Canada

2018 ◽  
Vol 63 (2) ◽  
pp. e01679-18 ◽  
Author(s):  
Khadidja Yousfi ◽  
Christiane Gaudreau ◽  
Pierre A. Pilon ◽  
Brigitte Lefebvre ◽  
Matthew Walker ◽  
...  
Keyword(s):  
Sequence Analysis ◽  
Shigella Flexneri ◽  
Complete Sequence ◽  
Shigella Sonnei ◽  
Content Type ◽  
Genetic Mechanisms ◽  
Sex With Men

ABSTRACT We analyzed 254 Shigella species isolates collected in Québec, Canada, during 2013 and 2014. Overall, 23.6% of isolates showed reduced susceptibility to azithromycin (RSA) encoded by mphA (11.6%), ermB (1.7%), or both genes (86.7%). Shigella strains with RSA were mostly isolated from men who have sex with men (68.8% or higher) from the Montreal region. A complete sequence analysis of six selected plasmids from Shigella sonnei and different serotypes of Shigella flexneri emphasized the role of IS26 in the dissemination of RSA.

scholarly journals Shigella flexneri Phagosomal Escape Is Independent of Invasion

2007 ◽  
Vol 75 (10) ◽  
pp. 4826-4830 ◽  
Author(s):  
Susanne Paetzold ◽  
Sebastian Lourido ◽  
Bärbel Raupach ◽  
Arturo Zychlinsky
Keyword(s):  
Cell Invasion ◽  
Type Iii Secretion ◽  
Shigella Flexneri ◽  
Mucosal Inflammation ◽  
Virulence Plasmid ◽  
Secretion Systems ◽  
Type Iii Secretion Systems ◽  
Macrophage Cytotoxicity ◽  
Serovar Typhimurium ◽  
Epithelial Cell Invasion

ABSTRACT Infections with Salmonella enterica serovar Typhimurium and Shigella flexneri result in mucosal inflammation in response to epithelial cell invasion and macrophage cytotoxicity. These processes are mediated by type III secretion systems encoded in homologous virulence loci in the two species, namely, Salmonella pathogenicity island 1 (SPI-1), carried in the genome, and the Shigella entry region (SER), carried in a large virulence plasmid. Here we show that SPI-1 can functionally complement a deletion of SER in S. flexneri, restoring invasion of epithelial cells, macrophage cytotoxicity, and phagosomal escape. Furthermore, S. flexneri phagosomal escape requires the SER and another gene(s) carried on the large virulence plasmid. We demonstrate that the processes of invasion and phagosomal escape can be uncoupled in S. flexneri.

scholarly journals Virulent Shigella flexneri subverts the host innate immune response through manipulation of antimicrobial peptide gene expression

2008 ◽  
Vol 205 (5) ◽  
pp. 1121-1132 ◽  
Author(s):  
Brice Sperandio ◽  
Béatrice Regnault ◽  
Jianhua Guo ◽  
Zhi Zhang ◽  
Samuel L. Stanley ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Shigella Flexneri ◽  
Host Cells ◽  
Virulence Plasmid ◽  
Cationic Peptides ◽  
Immunity Genes ◽  
Genes Encoding ◽  
Peptide Gene

Antimicrobial factors are efficient defense components of the innate immunity, playing a crucial role in the intestinal homeostasis and protection against pathogens. In this study, we report that upon infection of polarized human intestinal cells in vitro, virulent Shigella flexneri suppress transcription of several genes encoding antimicrobial cationic peptides, particularly the human β-defensin hBD-3, which we show to be especially active against S. flexneri. This is an example of targeted survival strategy. We also identify the MxiE bacterial regulator, which controls a regulon encompassing a set of virulence plasmid-encoded effectors injected into host cells and regulating innate signaling, as being responsible for this dedicated regulatory process. In vivo, in a model of human intestinal xenotransplant, we confirm at the transcriptional and translational level, the presence of a dedicated MxiE-dependent system allowing S. flexneri to suppress expression of antimicrobial cationic peptides and promoting its deeper progression toward intestinal crypts. We demonstrate that this system is also able to down-regulate additional innate immunity genes, such as the chemokine CCL20 gene, leading to compromised recruitment of dendritic cells to the lamina propria of infected tissues. Thus, S. flexneri has developed a dedicated strategy to weaken the innate immunity to manage its survival and colonization ability in the intestine.

scholarly journals Evaluation with an iuc::Tn10 mutant of the role of aerobactin production in the virulence of Shigella flexneri.

1987 ◽  
Vol 55 (9) ◽  
pp. 1963-1969 ◽  
Author(s):  
X Nassif ◽  
M C Mazert ◽  
J Mounier ◽  
P J Sansonetti
Keyword(s):  
Shigella Flexneri

scholarly journals Possible role of colonic content in the mucosal association of pathogenic shigella

1980 ◽  
Vol 29 (3) ◽  
pp. 1197-1199
Author(s):  
R Prizont ◽  
W P Reed
Keyword(s):  
Shigella Flexneri ◽  
Colonic Content

Association of Shigella flexneri to cecal membrances was studied by incubating the pathogen with cecal slices of germfree mice. The slices were first incubated with stool supernatants from germfree, shigella-monocontaminated, and conventional animals. Quantitation of shigellae in homogenates of treated slices revealed an increase of organisms only in those slices exposed to contaminated stool supernatants.

scholarly journals The dual role of candida glabrata drug:H+ antiporter CgAqr1 (ORF CAGL0J09944g) in antifungal drug and acetic acid resistance

2013 ◽  
Vol 4 ◽  
Author(s):  
Catarina Costa ◽  
André Henriques ◽  
Carla Pires ◽  
Joana Nunes ◽  
Michiyo Ohno ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Candida Glabrata ◽  
Acid Resistance ◽  
Dual Role ◽  
Antifungal Drug ◽  
Acetic Acid Resistance

scholarly journals Role of attP in Integrase-Mediated Integration of the Shigella Resistance Locus Pathogenicity Island of Shigella flexneri

2004 ◽  
Vol 48 (3) ◽  
pp. 1028-1031 ◽  
Author(s):  
Sally A. Turner ◽  
Shelley N. Luck ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Ben Adler
Keyword(s):  
Shigella Flexneri ◽  
Pathogenicity Island ◽  
Resistance Locus ◽  
Site Specific ◽  
Site Specific Recombination ◽  
Independent Site

ABSTRACT The Shigella resistance locus (SRL) pathogenicity island (PAI) in Shigella spp. mediates resistance to streptomycin, ampicillin, chloramphenicol, and tetracycline. It can be excised from the chromosome via site-specific recombination mediated by the P4-related int gene. Here, we show that SRL PAI attP is capable of RecA-independent, site-specific, int-mediated integration into two bacterial tRNA attB sites.

scholarly journals Genetic functions of the NAIP family of inflammasome receptors for bacterial ligands in mice

2016 ◽  
Vol 213 (5) ◽  
pp. 647-656 ◽  
Author(s):  
Yue Zhao ◽  
Jianjin Shi ◽  
Xuyan Shi ◽  
Yupeng Wang ◽  
Fengchao Wang ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Type Iii Secretion ◽  
Physiological Function ◽  
Shigella Flexneri ◽  
Critical Role ◽  
Bacterial Virulence ◽  
Infection Model ◽  
Inflammasome Activation ◽  
Inflammatory Damage

Biochemical studies suggest that the NAIP family of NLR proteins are cytosolic innate receptors that directly recognize bacterial ligands and trigger NLRC4 inflammasome activation. In this study, we generated Naip5−/−, Naip1−/−, and Naip2−/− mice and showed that bone marrow macrophages derived from these knockout mice are specifically deficient in detecting bacterial flagellin, the type III secretion system needle, and the rod protein, respectively. Naip1−/−, Naip2−/−, and Naip5−/− mice also resist lethal inflammasome activation by the corresponding ligand. Furthermore, infections performed in the Naip-deficient macrophages have helped to define the major signal in Legionella pneumophila, Salmonella Typhimurium and Shigella flexneri that is detected by the NAIP/NLRC4 inflammasome. Using an engineered S. Typhimurium infection model, we demonstrate the critical role of NAIPs in clearing bacterial infection and protecting mice from bacterial virulence–induced lethality. These results provide definitive genetic evidence for the important physiological function of NAIPs in antibacterial defense and inflammatory damage–induced lethality in mice.

scholarly journals Deacidification by FhlA-dependent hydrogenase is involved in urease activity and urinary stone formation in uropathogenic Proteus mirabilis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Wen-Yuan Lin ◽  
Shwu-Jen Liaw
Keyword(s):  
Proteus Mirabilis ◽  
Urease Activity ◽  
Stone Formation ◽  
Large Subunit ◽  
Acid Resistance ◽  
Urinary Stone ◽  
Potential Strategy ◽  
Ph Range ◽  
Tract Infections

Abstract Proteus mirabilis is an important uropathogen, featured with urinary stone formation. Formate hydrogenlyase (FHL), consisting of formate dehydrogenase H and hydrogenase for converting proton to hydrogen, has been implicated in virulence. In this study, we investigated the role of P. mirabilis FHL hydrogenase and the FHL activator, FhlA. fhlA and hyfG (encoding hydrogenase large subunit) displayed a defect in acid resistance. fhlA and hyfG mutants displayed a delay in medium deacidification compared to wild-type and ureC mutant failed to deacidify the medium. In addition, loss of fhlA or hyfG decreased urease activity in the pH range of 5–8. The reduction of urease activities in fhlA and hyfG mutants subsided gradually over the pH range and disappeared at pH 9. Furthermore, mutation of fhlA or hyfG resulted in a decrease in urinary stone formation in synthetic urine. These indicate fhlA- and hyf-mediated deacidification affected urease activity and stone formation. Finally, fhlA and hyfG mutants exhibited attenuated colonization in mice. Altogether, we found expression of fhlA and hyf confers medium deacidification via facilitating urease activity, thereby urinary stone formation and mouse colonization. The link of acid resistance to urease activity provides a potential strategy for counteracting urinary tract infections by P. mirabilis.

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