Presence or Absence of Lipopolysaccharide O Antigens Affects Type III Secretion by
            <i>Pseudomonas aeruginosa</i>

Augustin, D. K.; Song, Yuanlin; Baek, Marshall; Sawa, Yoriko; Singh, Gaurav; Taylor, Benjamin; Rubio-Mills, Amua; Flanagan, Judith; Wiener-Kronish, Jeanine P.; Lynch, Susan V.

doi:10.1128/jb.01839-06

Cited by 55 publications

(58 citation statements)

References 33 publications

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“…TTSS activity and the length of O-antigen side chains seem to be linked in pathogenic bacteria: in Shigella flexneri, glucosylation of O antigen resulting in a shorter polymeric O-antigen region enhanced TTSS function (45). In P. aeruginosa, increased virulence could be detected in an Oantigen mutant that induced significantly increased lung damage compared to that of the wild type (2). Phospholipase A expression and its secretion into the medium by a TTSS were increased in an O-antigen-negative strain of Yersinia enterocolitica (4).…”

Section: Vol 77 2009 O-antigen-negative Serovar Typhimurium Elicitsmentioning

confidence: 71%

“…Additionally, the ⌬wbaP mutant (SKI12) showed a severe defect in motility. There are several other reports connecting LPS mutations with a loss in motility: in serovar Typhimurium, addition of a monoclonal anti-LPS antibody to a diluted bacterial culture led to instant paralysis of the bacteria (8), and in a Pseudomonas aeruginosa ⌬waaL strain, a severe impairment in motility was detected (2). Also, an Escherichia coli mutant lacking O antigen was reported to show a nonmotile phenotype (37).…”

Section: Discussionmentioning

confidence: 99%

“…The TTSS-1 (inv-spa) is a major Salmonella virulence factor required for the induction of membrane ruffling and invasion of nonphagocytic cells. In Shigella flexneri and Pseudomonas aeruginosa, the activity of TTSS is known to be modulated by the length of the O side chain of LPS (2,45). Therefore, we tested the functionality of TTSS-1 in the Oantigen-deficient ⌬wbaP strain (SKI12) using an in vitro inva- :pKI9 whole-cell extracts treated with proteinase K. This confirms the lack of polymeric O antigen in the ⌬wbaP strain (SKI12), its restoration in the ⌬wbaP::pKI9 strain (SKI33), and normal expression of ECA (right).…”

Section: Resultsmentioning

confidence: 99%

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O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

et al. 2009

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Lipopolysaccharide (LPS) is a major constituent of the outer membrane and an important virulence factor of Salmonella enterica subspecies 1 serovar Typhimurium (serovar Typhimurium). To evaluate the role of LPS in eliciting intestinal inflammation in streptomycin-treated mice, we constructed an O-antigen-deficient serovar Typhimurium strain through deletion of the wbaP gene. The resulting strain was highly susceptible to human complement activity and the antimicrobial peptide mimic polymyxin B. Furthermore, it showed a severe defect in motility and an attenuated phenotype in a competitive mouse infection experiment, where the ⌬wbaP strain (SKI12) was directly compared to wild-type Salmonella. Nevertheless, the ⌬wbaP strain (SKI12) efficiently invaded HeLa cells in vitro and elicited acute intestinal inflammation in streptomycin-pretreated mice. Our experiments prove that the presence of complete LPS is not essential for in vitro invasion or for triggering acute colitis.

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Section: Vol 77 2009 O-antigen-negative Serovar Typhimurium Elicitsmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

et al. 2009

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“…In the context of cystic fibrosis infection, mucoidy favours the formation of protected colonies with increased resistance to opsonization, phagocytosis and destruction by antibiotics (Pritt et al, 2007). It has been shown that alterations of a single band or both bands of the O-antigen of P. aeruginosa PAO1 can give rise to mutants with increased cytotoxicity mediated by the type III secretion system (Augustin et al, 2007). In addition, changes in O-polysaccharide expression in PAO1 affect the size and protein content of outer membrane vesicles, and the formation of a robust biofilm (Murphy et al, 2014).…”

Section: Cross-resistance and Reversibility Of Mutantsmentioning

confidence: 99%

Pseudolysogeny and sequential mutations build multiresistance to virulent bacteriophages in Pseudomonas aeruginosa

Latino

2016

Microbiology

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Coevolution between bacteriophages (phages) and their prey is the result of mutualistic interactions. Here, we show that pseudolysogeny is a frequent outcome of infection by virulent phages of Pseudomonas aeruginosa and that selection of resistant bacterial mutants is favoured by continuous production of phages. We investigated the frequency and characteristics of P. aeruginosa strain PAO1 variants resisting infection by different combinations of virulent phages belonging to four genera. The frequency of resistant bacteria was 10 25 for single phage infection and 10 26 for infections with combinations of two or four phages. The genome of 27 variants was sequenced and the comparison with the genome of the parental PAO1 strain allowed the identification of point mutations or small indels. Four additional variants were characterized by a candidate gene approach. In total, 27 independent mutations were observed affecting 14 genes and a regulatory region. The mutations affected genes involved in biosynthesis of type IV pilus, alginate, LPS and O-antigen. Half of the variants possessed changes in homopolymer tracts responsible for frameshift mutations and these phase variation mutants were shown to be unstable. Eleven double mutants were detected. The presence of free phage DNA was observed in association with exclusion of superinfection in half of the variants and no chromosomal mutation could be found in three of them. Upon further growth of these pseudolysogens, some variants with new chromosomal mutations were recovered, presumably due to continuous evolutionary pressure.

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“…Single and combined deletion strains of PAK and PA103 permitted analysis of the contribution of each of the four known P. aeruginosa type III exotoxins to endothelial permeability. As previously described, the ability of wild-type and mutant bacterial strains to produce exotoxins was confirmed by Western blot using antibodies against ExoU, ExoS, and ExoT (19). For endothelial permeability studies, strains were cultured overnight in 5 ml of LB medium before dilution with sterile PBS to a final cell count of 1 3 10 9 cells ml 21 (determined by OD 600 readings).…”

Section: Recombinant Hsp72 Adenovirusmentioning

confidence: 99%

Role of Small GTPases and αvβ5 Integrin in Pseudomonas aeruginosa–Induced Increase in Lung Endothelial Permeability

Ganter¹,

Roux²,

Su³

et al. 2009

Am J Respir Cell Mol Biol

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Pseudomonas aeruginosa is an opportunistic pathogen that can cause severe pneumonia associated with airspace flooding with proteinrich edema in critically ill patients. The type III secretion system is a major virulence factor and contributes to dissemination of P. aeruginosa. However, it is still unknown which particular bacterial toxin and which cellular pathways are responsible for the increase in lung endothelial permeability induced by P. aeruginosa. Thus, the first objective of this study was to determine the mechanisms by which this species causes an increase in lung endothelial permeability. The results showed that ExoS and ExoT, two of the four known P. aeruginosa type III cytotoxins, were primarily responsible for bacterium-induced increases in protein permeability across the lung endothelium via an inhibition of Rac1 and an activation of the RhoA signaling pathway. In addition, inhibition of the avb5 integrin, a central regulator of lung vascular permeability, prevented these P. aeruginosa-mediated increases in albumin flux due to endothelial permeability. Finally, prior activation of the stress protein response or adenoviral gene transfer of the inducible heat shock protein Hsp72 also inhibited the damaging effects of P. aeruginosa on the barrier function of lung endothelium. Taken together, these results demonstrate the critical role of the RhoA/avb5 integrin pathway in mediating P. aeruginosa-induced lung vascular permeability. In addition, activation of the stress protein response with pharmacologic inhibitors of Hsp90 may protect lungs against P. aeruginosainduced permeability changes.Keywords: lung; Pseudomonas aeruginosa; endothelial cells; integrin; heat shock response Pseudomonas aeruginosa is an opportunistic pathogen that causes lethal pneumonia in immunocompromised individuals and in critically ill patients (1). The high mortality of patients who develop P. aeruginosa pneumonia is associated with the development of acute lung injury, characterized by the flooding of the airspaces with a protein-rich edema. P. aeruginosa can cause lung damage by multiple mechanisms. Flagella, pili, and lipopolysaccharide are the initial tethers that facilitate bacterial cell contact by binding the cell surface glycolipid asialo-GM1 (2). Upon cell contact, the type III secretion system allows P. aeruginosa to inject toxins into the cells. Four of these effector proteins, ExoY, ExoS, ExoT, and ExoU, are known to be key determinants of virulence in this bacterium and can lead to host cell destruction and dissemination of P. aeruginosa (3, 4). Other virulence factors associated with P. aeruginosa include elastase, alkaline phosphatase, exotoxin A, and phospholipase, secreted by the type II secretion system, which also participate in host cell invasion by this bacterium (5). In addition, pyoverdin, pyochelin, and pyocyanin, secreted metabolites associated with generation of reactive oxygen species, also are involved in P. aeruginosa-induced host cell injury (5).Multiple in vivo studies have shown that P. aerugin...

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Presence or Absence of Lipopolysaccharide O Antigens Affects Type III Secretion by Pseudomonas aeruginosa

Cited by 55 publications

References 33 publications

O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

O-Antigen-NegativeSalmonella entericaSerovar Typhimurium Is Attenuated in Intestinal Colonization but Elicits Colitis in Streptomycin-Treated Mice

Pseudolysogeny and sequential mutations build multiresistance to virulent bacteriophages in Pseudomonas aeruginosa

Role of Small GTPases and αvβ5 Integrin in Pseudomonas aeruginosa–Induced Increase in Lung Endothelial Permeability

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