Type II Antitoxin HigA Is a Key Virulence Regulator in Pseudomonas aeruginosa

2021 ◽  
Author(s):  
Yingjie Song ◽  
Siping Zhang ◽  
Guihua Luo ◽  
Yalin Shen ◽  
Changcheng Li ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Type Ii ◽  
Virulence Regulator

scholarly journals Identification of type II and type III pyoverdine receptors from Pseudomonas aeruginosa

Microbiology ◽  
2003 ◽  
Vol 149 (4) ◽  
pp. 821-831 ◽  
Author(s):  
Magaly de Chial ◽  
Bart Ghysels ◽  
Scott A. Beatson ◽  
Valérie Geoffroy ◽  
Jean Marie Meyer ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Type Ii ◽  
Type Iii

scholarly journals Resistance Mechanisms of Multiresistant Pseudomonas aeruginosa Strains from Germany and Correlation with Hypermutation

2007 ◽  
Vol 51 (11) ◽  
pp. 4062-4070 ◽  
Author(s):  
B. Henrichfreise ◽  
I. Wiegand ◽  
W. Pfister ◽  
B. Wiedemann
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Efflux Pump ◽  
Acquired Resistance ◽  
Resistance Mechanisms ◽  
Type Ii ◽  
Mechanisms Of Resistance ◽  
Resistance Determinants ◽  
Class 1 ◽  
Mutator Strains ◽  
Multiresistant Strains

ABSTRACT In this study, we analyzed the mechanisms of multiresistance for 22 clinical multiresistant and clonally different Pseudomonas aeruginosa strains from Germany. Twelve and 10 strains originated from cystic fibrosis (CF) and non-CF patients, respectively. Overproduction of the efflux systems MexAB-OprM, MexCD-OprJ, MexEF-OprN, and MexXY-OprM was studied. Furthermore, loss of OprD, alterations in type II topoisomerases, AmpC overproduction, and the presence of 25 acquired resistance determinants were investigated. The presence of a hypermutation phenotype was also taken into account. Besides modifications in GyrA (91%), the most frequent mechanisms of resistance were MexXY-OprM overproduction (82%), OprD loss (82%), and AmpC overproduction (73%). Clear differences between strains from CF and non-CF patients were found: numerous genes coding for aminoglycoside-modifying enzymes and located, partially in combination with β-lactamase genes, in class 1 integrons were found only in strains from non-CF patients. Furthermore, multiple modifications in type II topoisomerases conferring high quinolone resistance levels and overexpression of MexAB-OprM were exclusively detected in multiresistant strains from non-CF patients. Correlations of the detected phenotypes and resistance mechanisms revealed a great impact of efflux pump overproduction on multiresistance in P. aeruginosa. Confirming previous studies, we found that additional, unknown chromosomally mediated resistance mechanisms remain to be determined. In our study, 11 out of 12 strains and 3 out of 10 strains from CF patients and non-CF patients, respectively, were hypermutable. This extremely high proportion of mutator strains should be taken into consideration for the treatment of multiresistant P. aeruginosa.

scholarly journals Diversity, Prevalence, and Longitudinal Occurrence of Type II Toxin-Antitoxin Systems of Pseudomonas aeruginosa Infecting Cystic Fibrosis Lungs

2017 ◽  
Vol 8 ◽  
Author(s):  
Sandra B. Andersen ◽  
Melanie Ghoul ◽  
Ashleigh S. Griffin ◽  
Bent Petersen ◽  
Helle K. Johansen ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Type Ii

scholarly journals Role of fimV in type II secretion system-dependent protein secretion of Pseudomonas aeruginosa on solid medium

Microbiology ◽  
2011 ◽  
Vol 157 (7) ◽  
pp. 1945-1954 ◽  
Author(s):  
Gérard P. F. Michel ◽  
Anthony Aguzzi ◽  
Geneviève Ball ◽  
Chantal Soscia ◽  
Sophie Bleves ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Solid Medium ◽  
Early Stage ◽  
Growth Conditions ◽  
Classical Type ◽  
Type Ii Secretion ◽  
Type Ii ◽  
Secretion Systems ◽  
Type Ii Secretion System ◽  
Dependent Protein

Although classical type II secretion systems (T2SSs) are widely present in Gram-negative bacteria, atypical T2SSs can be found in some species. In Pseudomonas aeruginosa, in addition to the classical T2SS Xcp, it was reported that two genes, xphA and xqhA, located outside the xcp locus were organized in an operon (PaQa) which encodes the orphan PaQa subunit. This subunit is able to associate with other components of the classical Xcp machinery to form a functional hybrid T2SS. In the present study, using a transcriptional lacZ fusion, we found that the PaQa operon was more efficiently expressed (i) on solid LB agar than in liquid LB medium, (ii) at 25 °C than at 37 °C and (iii) at an early stage of growth. These results suggested an adaptation of the hybrid system to particular environmental conditions. Transposon mutagenesis led to the finding that vfr and fimV genes are required for optimal expression of the orphan PaQa operon in the defined growth conditions used. Using an original culturing device designed to monitor secretion on solid medium, the ring-plate system, we found that T2SS-dependent secretion of exoproteins, namely the elastase LasB, was affected in a fimV deletion mutant. Our findings led to the discovery of an interplay between FimV and the global regulator Vfr triggering the modulation of the level of Vfr and consequently the modulation of T2SS-dependent secretion on solid medium.

scholarly journals Interaction domains in the Pseudomonas aeruginosa type II secretory apparatus component XcpS (GspF)

Microbiology ◽  
2007 ◽  
Vol 153 (5) ◽  
pp. 1582-1592 ◽  
Author(s):  
Jorik Arts ◽  
Arjan de Groot ◽  
Geneviève Ball ◽  
Eric Durand ◽  
Mohammed El Khattabi ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Type Ii ◽  
Interaction Domains ◽  
Secretory Apparatus

scholarly journals Type II Topoisomerase Mutations in Ciprofloxacin-Resistant Strains of Pseudomonas aeruginosa

1999 ◽  
Vol 43 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Hyam Mouneimné ◽  
Jérome Robert ◽  
Vincent Jarlier ◽  
Emmanuelle Cambau
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Novel Mutation ◽  
Geometric Mean ◽  
Quinolone Resistance ◽  
Single Mutation ◽  
Type Ii ◽  
Wild Type ◽  
Clinical Strains ◽  
Major Mechanism ◽  
Resistant Strains

ABSTRACT We determined the sequences of the quinolone resistance-determining regions of gyrA, gyrB, and parCgenes for 30 clinical strains of Pseudomonas aeruginosaresistant to ciprofloxacin that were previously complemented by wild-type gyrA and gyrB plasmid-borne alleles and studied for their coresistance to imipenem (E. Cambau, E. Perani, C. Dib, C. Petinon, J. Trias, and V. Jarlier, Antimicrob. Agents Chemother. 39:2248–2252, 1995). In the present study, we found mutations in type II topoisomerase genes for all strains. Twenty-eight strains had a missense mutation in gyrA (codon 83 or 87). Ten of them had an additional mutation in parC(codon 80 or 84), including a novel mutation of Ser-80 to Trp, but all were fully complemented by a plasmid-borne wild-type gyrAallele. The remaining two strains harbored the first gyrBmutation described in P. aeruginosa, leading to the substitution of phenylalanine for serine 464. The strains which had two mutations in type II topoisomerase genes (i.e.,gyrA and parC) were significantly more resistant to fluoroquinolones than those with a single mutation ingyrA or gyrB (geometric mean MICs of ciprofloxacin, 39.4 versus 10.9 μg/ml, P < 0.01; geometric mean MICs of sparfloxacin, 64.0 versus 22.6,P < 0.01). No mutant with a parC mutation alone was observed, which favors DNA gyrase being the primary target for fluoroquinolones. These results demonstrate that gyrAmutations are the major mechanism of resistance to fluoroquinolones for clinical strains of P. aeruginosa and that additional mutations in parC lead to a higher level of quinolone resistance.

O2- and pneumonia-induced lung injury. II. Properties of pulmonary surfactant

1989 ◽  
Vol 67 (1) ◽  
pp. 357-365 ◽  
Author(s):  
R. J. King ◽  
J. J. Coalson ◽  
J. J. Seidenfeld ◽  
A. R. Anzueto ◽  
D. B. Smith ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lung Injury ◽  
Pulmonary Surfactant ◽  
Phospholipid Composition ◽  
Lung Mechanics ◽  
Type Ii ◽  
Biochemical Modification ◽  
Type Ii Cell ◽  
Normal Composition ◽  
Substantial Change

Pulmonary surfactant was isolated from the lavage fluids of animals during the course of exposure to 100% O2, 80% O2, 40% O2, or 80% O2 plus 10(8) Pseudomonas aeruginosa instilled intratracheally and analyzed for its phospholipid composition. After 4–5 days of exposure to 100% O2, disaturated phophatidylcholine (DSPC) decreased to 87% of control, whereas the ratio of phosphatidylglycerol to phosphatidylinositol (PG/PI) was 37% of control. Longer periods of ventilation with 100% O2 resulted in DSPC falling to less than 40% of control. The injury was not reversed by reducing the O2 to 50%; rather, a progressive deterioration ensued. Acute respiratory failure (ARF) induced by 5 days of bacterial infection was very similar to that seen after 5 days of exposure to 100% O2. Ventilation with 80% O2 for 6 days resulted in smaller changes in DSPC but with differences in PG/PI comparable to those seen with 100% O2 or infection. We conclude that the ability of the type II cell to synthesize surfactant of normal composition is significantly impaired in these models of ARF. The earliest index of biochemical modification is the substantial change in PG/PI, which may be predictive of early lung injury. Further exacerbation of the injury could result in the reduction of DSPC content, with subsequent changes in lung mechanics and gas exchange.

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