Regulation of the <i>xcp</i> secretion pathway by multiple quorum‐sensing modulons in <i>Pseudomonas aeruginosa</i>

Chapon, Virginie; Akrim, Mohammed; Latifi, Amel; Williams, Paul; Lazdunski, Andrée; Bally, Marc

doi:10.1046/j.1365-2958.1997.4271794.x

Cited by 129 publications

(89 citation statements)

References 44 publications

(74 reference statements)

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“…In contrast to the progress made toward elucidating the components of the type II secretion apparatus, there are few data on the regulation of its genes, although quorum sensing has been linked to xcp expression in Pseudomonas aeruginosa (15,73,74). While demonstrating that L. pneumophila piliation is temperature regulated, our laboratory observed an increase in the level of pilD-containing transcripts when wild-type legionellae were grown at 30 versus 37°C (48).…”

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confidence: 79%

The Type II Protein Secretion System of Legionella pneumophila Promotes Growth at Low Temperatures

2004

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The gram-negative bacterium Legionella pneumophila grows in both natural and man-made water systems and in the mammalian lung as a facultative intracellular parasite. The PilD prepilin peptidase of L. pneumophila promotes type IV pilus biogenesis and type II protein secretion. Whereas pili enhance adherence, Legionella type II secretion is critical for intracellular growth and virulence. Previously, we observed that pilD transcript levels are greater in legionellae grown at 30 versus 37°C. Using a new pilD::lacZ fusion strain, we now show that pilD transcriptional initiation increases progressively as L. pneumophila is grown at 30, 25, and 17°C. Legionella pilD mutants also had a dramatically reduced ability to grow in broth and to form colonies on agar at the lower temperatures. Whereas strains specifically lacking type IV pili were not defective for lowtemperature growth, mutations in type II secretion (lsp) genes greatly impaired the capacity of L. pneumophila to form colonies at 25, 17, and 12°C. Indeed, the lsp mutants were completely unable to grow at 12°C. The growth defect of the pilD and lsp mutants was complemented by reintroduction of the corresponding intact gene. Interestingly, the lsp mutants displayed improved growth at 25°C when plated next to a streak of wild-type but not mutant bacteria, implying that a secreted, diffusible factor promotes low-temperature growth. Mutants lacking either the known secreted acid phosphatases, lipases, phospholipase C, lysophospholipase A, or protease grew normally at 25°C, suggesting the existence of a critical, yet-to-be-defined exoprotein(s). In summary, these data document, for the first time, that L. pneumophila replicates at temperatures below 20°C and that a bacterial type II protein secretion system facilitates growth at low temperatures.

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confidence: 79%

The Type II Protein Secretion System of Legionella pneumophila Promotes Growth at Low Temperatures

2004

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“…One group includes the exotoxin ExoA and diverse degrading enzymes such as proteases and lipases, which are released into the environment by the type II protein secretion system Xcp. The expression of the Xcp machinery and the cognate substrates are positively regulated by autoinducer systems (Gambello et al, 1993;Chapon-Herve et al, 1997). The second group of secreted pathogenicity factors comprises cellular modulins such as the exotoxins ExoS, T, U and Y, which are secreted and translocated into host cells through an 'injection needle' of the TTSS (Psc apparatus), known as the exoenzyme S regulon.…”

Section: Discussionmentioning

confidence: 99%

Expression of Pseudomonas aeruginosa exoS is controlled by quorum sensing and RpoS

et al. 2004

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In Pseudomonas aeruginosa, virulence determinants and biofilm formation are coordinated via a hierarchical quorum sensing cascade, which involves the transcriptional regulators LasR and RhlR and their cognate homoserine lactone activators C12-HSL [N-(3-oxododecanoyl)-L-homoserine lactone] and C4-HSL (N-butanoyl-L-homoserine lactone), which are produced by LasI and RhlI, respectively. The exoenzyme S regulon of P. aeruginosa, comprises genes for a type III secretion system and for four anti-host effector proteins (ExoS, T, U and Y), which are translocated into host cells. It is a reasonable assumption that this ExoS regulon should be downregulated in the biofilm growth state and thus should also be under the regulatory control of the Las/Rhl system. Therefore, an exoS9-gfp reporter construct was used, and the influence of the Las and Rhl quorum sensing systems and the effect of the stationary-phase sigma factor RpoS on regulation of the exoS gene was examined. Evidence is provided for downregulation of exoS during biofilm formation of P. aeruginosa PAO1. The rhlI mutant PDO100 and rhlR mutant PDO111, but not the lasI mutant PDO-JP1, showed approximately twofold upregulation of the exoS9-gfp reporter in comparison to PAO1. Upregulation of exoS9-gfp in the PDO100 mutant could be repressed to normal level by adding C4-HSL autoinducer, indicating a negative regulatory effect of RhlR/C4-HSL on exoS expression. As RhlR/C4-HSL is also involved in regulation of RpoS, the P. aeruginosa rpoS mutant SS24 was examined and the exoS9-gfp reporter was found to be fivefold upregulated in comparison to PAO1. For the first time evidence is reported for a regulatory cascade linking RhlR/RhlI and RpoS with the expression of the anti-host effector ExoS, part of the exoenzyme S regulon. Moreover, these data suggest that the exoenzyme S regulon may be downregulated in P. aeruginosa biofilms. INTRODUCTIONPseudomonas aeruginosa, an increasingly prevalent opportunistic human pathogen, is the most common Gram-negative bacterium found in infections of immunocompromised patients and of individuals suffering from cystic fibrosis (CF). Once P. aeruginosa has taken residence in the lungs of CF patients, it contributes substantially to morbidity and mortality in this population. The pseudomonads, which are seldom eradicated by antibacterial chemotherapy, chronically colonize the bronchoalveolar lumen of CF lungs and lead to recurrent pulmonal exacerbations, resulting in a progressive decline in lung function. Various virulence determinants have been shown to play a role in the pathogenesis of P. aeruginosa. The production of multiple of these virulence factors, including elastase, alkaline protease, LasA protease, phospholipase C, exotoxin A, rhamnolipid and pyocyanin relies on a cell-tocell communication system known as quorum sensing (van Delden & Iglewski, 1998;Winzer & Williams, 2001). These regulatory systems enable P. aeruginosa to produce virulence factors in a coordinated, cell-density-dependent manner. P. aeruginosa contains two separat...

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“…In P. aeruginosa there are at least two different quorum sensing systems : las and rhl (Gambello & Iglewski, 1991 ;Seed et al, 1995 ;Ochsner & Reiser, 1995), which code for synthetases (LasI\RhlI) and cognate transcriptional regulators (LasR\RhlR). The lasI-lasR system has been shown to modulate expression of lasI itself (Seed et al, 1995), lasB (elastase) (Passador et al, 1993 ;Pearson et al, 1997), lasA (Staphylolytic protease) , apr (alkaline protease) , the xcp secretion pathway (Chapon-Herve et al, 1997), twitching motility (Glessner et al, 1999) and rhlR (Latifi et al, 1996 ;. The rhlI-rhlR system modulates expression of rhlI itself (Latifi et al, 1996), rhlAB (rhamnolipid biosynthesis) (Ochsner & Reiser, 1995 ;Pearson et al, 1997), lasB (elastase) (Brint & Ohman, 1995 ;Pearson et al, 1995, twitching motility (Glessner et al, 1999) and rpoS (Latifi et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Pseudomonas aeruginosa mutations in lasI and rhlI quorum sensing systems result in milder chronic lung infection

et al. 2001

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To understand the importance of quorum sensing in chronic Pseudomonas aeruginosa lung infection, the in vivo pathogenic effects of the wild-type P. aeruginosa PAO1 and its double mutant, PAO1 lasI rhlI, in which the signalgenerating parts of the quorum sensing systems are defective were compared. The rat model of P. aeruginosa lung infection was used in the present study. The rats were killed on days 3, 7, 14 and 28 after infection with the P. aeruginosa strains. The results showed that during the early stages of infection, the PAO1 double mutant induced a stronger serum antibody response, higher production of pulmonary interferon γ, and more powerful blood polymorphonuclear leukocyte (PMN) chemiluminescence compared to its wild-type counterpart. On days 14 and 28 post-infection, significantly milder lung pathology, a reduction in the number of mast cells present in the lung foci, a reduced number of lung bacteria, and minor serum IgG and IgG1 responses but increased lung interferon γ production were detected in the group infected with the PAO1 double mutant when compared with the PAO1-infected group. Delayed immune responses were observed in the PAO1-infected group and they might be associated with the production of virulence factors that are controlled by the quorum sensing systems. The conclusion of this study is that functional lasI and rhlI genes of P. aeruginosa PAO1 play a significant role during lung infection.

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Regulation of the xcp secretion pathway by multiple quorum‐sensing modulons in Pseudomonas aeruginosa

Cited by 129 publications

References 44 publications

The Type II Protein Secretion System of Legionella pneumophila Promotes Growth at Low Temperatures

The Type II Protein Secretion System of Legionella pneumophila Promotes Growth at Low Temperatures

Expression of Pseudomonas aeruginosa exoS is controlled by quorum sensing and RpoS

Pseudomonas aeruginosa mutations in lasI and rhlI quorum sensing systems result in milder chronic lung infection

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