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

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.

2018 ◽  
Vol 63 (2) ◽  
pp. e01679-18 ◽  
Author(s):  
Khadidja Yousfi ◽  
Christiane Gaudreau ◽  
Pierre A. Pilon ◽  
Brigitte Lefebvre ◽  
Matthew Walker ◽  
...  

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.


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

2004 ◽  
Vol 48 (3) ◽  
pp. 1028-1031 ◽  
Author(s):  
Sally A. Turner ◽  
Shelley N. Luck ◽  
Harry Sakellaris ◽  
Kumar Rajakumar ◽  
Ben Adler

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.


2016 ◽  
Vol 213 (5) ◽  
pp. 647-656 ◽  
Author(s):  
Yue Zhao ◽  
Jianjin Shi ◽  
Xuyan Shi ◽  
Yupeng Wang ◽  
Fengchao Wang ◽  
...  

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.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chang Niu ◽  
Jing Yang ◽  
Hongsheng Liu ◽  
Yong Cui ◽  
Huijie Xu ◽  
...  

2007 ◽  
Vol 88 (11) ◽  
pp. 3187-3197 ◽  
Author(s):  
Fleur Roberts ◽  
Gwen E. Allison ◽  
Naresh K. Verma

The temperate phage SfV encodes the genes responsible for the serotype conversion of Shigella flexneri strains from serotype Y to 5a. Bacteriophages often encode proteins that prevent subsequent infection by homologous phages; the mechanism by which this is accomplished is referred to as superinfection immunity. The serotype conversion mediated following lysogenization of SfV is one such mechanism. Another mechanism is the putative λ-like CI protein within SfV. This study reports the characterization of a third superinfection mechanism, transcription termination, in SfV. The presence of a small immunity-mediating RNA molecule, called CI RNA, and its essential role in the establishment of immunity, is shown. The novel role of the gene orf77, located immediately downstream from the transcription termination region, in inhibiting the establishment of CI RNA-mediated immunity is also presented.


2018 ◽  
Vol 86 (8) ◽  
Author(s):  
Erin Weddle ◽  
Hervé Agaisse

ABSTRACTShigella flexneridisseminates within the colonic mucosa by displaying actin-based motility in the cytosol of epithelial cells. Motile bacteria form membrane protrusions that project into adjacent cells and resolve into double-membrane vacuoles (DMVs) from which the bacteria escape, thereby achieving cell-to-cell spread. During dissemination,S. flexneriis targeted by LC3-dependent autophagy, a host cell defense mechanism against intracellular pathogens. TheS. flexneritype III secretion system effector protein IcsB was initially proposed to counteract the recruitment of the LC3-dependent autophagy machinery to cytosolic bacteria. However, a recent study proposed that LC3 was recruited to bacteria in DMVs formed during cell-to-cell spread. To resolve the controversy and clarify the role of autophagy inS. flexneriinfection, we tracked dissemination using live confocal microscopy and determined the spatial and temporal recruitment of LC3 to bacteria. This approach demonstrated that (i) LC3 was exclusively recruited to wild-type oricsBbacteria located in DMVs and (ii) theicsBmutant was defective in cell-to-cell spread due to failure to escape LC3-positive as well as LC3-negative DMVs. Failure ofS. flexnerito escape DMVs correlated with late LC3 recruitment, suggesting that LC3 recruitment is the consequence and not the cause of DMV escape failure. Inhibition of autophagy had no positive impact on the spreading of wild-type oricsBmutant bacteria. Our results unambiguously demonstrate that IcsB is required for DMV escape during cell-to-cell spread, regardless of LC3 recruitment, and do not support the previously proposed notion that autophagy countersS. flexneridissemination.


Microbiology ◽  
2004 ◽  
Vol 150 (4) ◽  
pp. 1079-1084 ◽  
Author(s):  
Bryn Edwards-Jones ◽  
Paul R. Langford ◽  
J. Simon Kroll ◽  
Jun Yu

Previously, the authors have shown that inactivation of Shigella flexneri yihE, a gene of unknown function upstream of dsbA, which encodes a periplasmic disulphide catalyst, results in a global change of gene expression. Among the severely down-regulated genes are galETKM, suggesting that the yihE mutant, Sh54, may inefficiently produce the UDP-glucose and UDP-galactose required for LPS synthesis. This paper demonstrates that LPS synthesis in Sh54 is impaired. As a result, Sh54 is unable to polymerize host cell actin, due to aberrant localization of IcsA, or to cause keratoconjunctivitis in guinea pigs. Furthermore, Sh54 is more sensitive to some antimicrobial agents, and exhibits epithelial cytotoxicity characteristic of neither wild-type nor dsbA mutants. Supplying galETK in trans restores LPS synthesis and corrects all the defects. Hence, it is clear that the Shigella yihE gene is important not only in regulating global gene expression, as shown previously, but also in virulence through LPS synthesis via regulating the expression of the galETK operon.


1995 ◽  
Vol 182 (3) ◽  
pp. 769-778 ◽  
Author(s):  
A Phalipon ◽  
M Kaufmann ◽  
P Michetti ◽  
J M Cavaillon ◽  
M Huerre ◽  
...  

To determine the role of humoral mucosal immune response in protection against shigellosis, we have obtained a monoclonal dimeric immunoglobulin A (IgA) antibody specific for Shigella flexneri serotype 5a lipopolysaccharide (mIgA) and used a murine pulmonary infection model that mimics the lesions occurring in natural intestinal infection. Adult BALB/c mice challenged with 10(7) S. flexneri organisms developed a rapid inflammatory response characterized by polymorphonuclear cell infiltration around and within the bronchi and strong systemic interleukin 6 response. Implantation of hybridoma cells in the back of mice, resulting in the development of a myeloma tumor producing mIgA in the serum and subsequently secretory mIgA in local secretions, or direct intranasal administration of these antibodies, protected the animals against subsequent intranasal challenge with S. flexneri serotype 5a. Absence of histopathological lesion and significant decrease in bacterial load of the lungs and of systemic interleukin 6 response were the three major criteria of protection. This protection was shown to be serotype-specific and dependent on local concentration of mIgA. These data demonstrate that mucosal antibodies directed against a single polysaccharidic surface epitope of Shigella can protect against the disease.


1988 ◽  
Vol 78 (11) ◽  
pp. 1432-1435 ◽  
Author(s):  
R V Tauxe ◽  
R C McDonald ◽  
N Hargrett-Bean ◽  
P A Blake

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