Journal articles: 'Lasb'

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Storey, Douglas G., Eva E. Ujack, Harvey R. Rabin, and Ian Mitchell. "Pseudomonas aeruginosa lasRTranscription Correlates with the Transcription of lasA,lasB, and toxA in Chronic Lung Infections Associated with Cystic Fibrosis." Infection and Immunity 66, no. 6 (June 1, 1998): 2521–28. http://dx.doi.org/10.1128/iai.66.6.2521-2528.1998.

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ABSTRACT The role of Pseudomonas aeruginosa quorum-sensing systems in the lung infections associated with cystic fibrosis (CF) has not been examined. The purpose of this study was to determine if genes regulated by the LasR-LasI quorum-sensing system were coordinately regulated by the P. aeruginosa populations during the lung infections associated with CF. We also wanted to ascertain if there was a relationship between the expression of lasR, a transcriptional regulator, and some P. aeruginosa virulence factors during these infections. We extracted RNAs from the bacterial populations of 131 sputa taken from 23 CF patients. These RNAs were blotted and hybridized with probes to P. aeruginosa lasA,lasB, and toxA. The hybridization signals from each probe were ranked, and the rankings were analyzed by a Spearman rank correlation to determine if there was an association between the population transcript accumulations for the three genes. The correlations between the transcript accumulation patterns of pairs of the genes suggested that lasA, lasB, andtoxA might be coordinately regulated during CF lung infections. To determine if this coordinate regulation might be due to regulation by LasR, we probed RNAs, extracted from 84 sputa, with thelasR, lasA, lasB, toxA, and algD probes. Statistical analysis indicated thatlasR transcript accumulation correlated tolasA, lasB, toxA, andalgD transcript accumulations. These results indicated thatlasR may at least partially regulate or be coordinately regulated with lasA, lasB, toxA, and algD during the lung infections associated with CF. These results also suggested that the LasR-LasI quorum-sensing system may control the expression of at least some virulence factors in the lungs of patients with CF.

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Kong, Kok-Fai, Suriya Ravi Jayawardena, Shalaka Dayaram Indulkar, Aimee del Puerto, Chong-Lek Koh, Niels Høiby, and Kalai Mathee. "Pseudomonas aeruginosa AmpR Is a Global Transcriptional Factor That Regulates Expression of AmpC and PoxB β-Lactamases, Proteases, Quorum Sensing, and Other Virulence Factors." Antimicrobial Agents and Chemotherapy 49, no. 11 (November 2005): 4567–75. http://dx.doi.org/10.1128/aac.49.11.4567-4575.2005.

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ABSTRACT In members of the family Enterobacteriaceae, ampC, which encodes a β-lactamase, is regulated by an upstream, divergently transcribed gene, ampR. However, in Pseudomonas aeruginosa, the regulation of ampC is not understood. In this study, we compared the characteristics of a P. aeruginosa ampR mutant, PAOampR, with that of an isogenic ampR + parent. The ampR mutation greatly altered AmpC production. In the absence of antibiotic, PAOampR expressed increased basal β-lactamase levels. However, this increase was not followed by a concomitant increase in the P ampC promoter activity. The discrepancy in protein and transcription analyses led us to discover the presence of another chromosomal AmpR-regulated β-lactamase, PoxB. We found that the expression of P. aeruginosa ampR greatly altered the β-lactamase production from ampC and poxB in Escherichia coli: it up-regulated AmpC but down-regulated PoxB activities. In addition, the constitutive P ampR promoter activity in PAOampR indicated that AmpR did not autoregulate in the absence or presence of inducers. We further demonstrated that AmpR is a global regulator because the strain carrying the ampR mutation produced higher levels of pyocyanin and LasA protease and lower levels of LasB elastase than the wild-type strain. The increase in LasA levels was positively correlated with the P lasA , P lasI , and P lasR expression. The reduction in the LasB activity was positively correlated with the P rhlR expression. Thus, AmpR plays a dual role, positively regulating the ampC, lasB, and rhlR expression levels and negatively regulating the poxB, lasA, lasI, and lasR expression levels.

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Anderson, Ronda M., Chad A. Zimprich, and Lynn Rust. "A Second Operator Is Involved in Pseudomonas aeruginosa Elastase (lasB) Activation." Journal of Bacteriology 181, no. 20 (October 15, 1999): 6264–70. http://dx.doi.org/10.1128/jb.181.20.6264-6270.1999.

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ABSTRACT Pseudomonas aeruginosa LasB elastase gene (lasB) transcription is controlled by the two-component quorum-sensing system of LasR, and the autoinducer, 3OC12-HSL (N-3-[oxododecanoyl]homoserine lactone). LasR and 3OC12-HSL-mediated lasBactivation requires a functional operator sequence (OP1) in thelasB promoter region. Optimal activation oflasB, however, requires a second sequence of 70% identity to OP1, named OP2, located 43 bp upstream of OP1. In this study, we used sequence substitutions and insertion mutations inlasBp-lacZ fusion plasmids to explore the role of OP2 in lasB activation. Our results demonstrate that (i) OP1 and OP2 synergistically mediate lasB activation; (ii) OP2, like OP1, responds to LasR and 3OC12-HSL; and (iii) the putative autoinducer-binding domain of LasR is not required for synergistic activation from OP1 and OP2.

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Cowell, Brigitte A., Sally S. Twining, Jeffrey A. Hobden, Mary S. F. Kwong, and Suzanne M. J. Fleiszig. "Mutation of lasA and lasB reduces Pseudomonas aeruginosa invasion of epithelial cells." Microbiology 149, no. 8 (August 1, 2003): 2291–99. http://dx.doi.org/10.1099/mic.0.26280-0.

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Pseudomonas aeruginosa is an opportunistic bacterial pathogen implicated in a variety of devastating conditions. Its flexibility as a pathogen is attributed to a myriad of virulence factors and regulatory elements that respond to prevailing environmental conditions. ExoS and ExoT are type III secreted effector proteins, regulated by the transcriptional activator ExsA, that can inhibit invasion of epithelial cells by cytotoxic strains of P. aeruginosa. This study sought to understand why invasive strains, which can secrete both ExoS and ExoT, still invade epithelial cells. The results showed that LasA and elastase (LasB), which are regulated by the Las and Rhl quorum-sensing systems, modulated P. aeruginosa invasion. Mutation of lasA and/or lasB reduced P. aeruginosa invasion, which was not fully restored by extracellularly added LasB, P. aeruginosa conditioned medium containing LasA and LasB, or EGTA pretreatment of cells. This indicated that protease effects on invasion involved factors additional to tight junction disruption and subsequent alterations to cell polarity. Upon mutation of lasA and/or lasB, steady-state levels of ExoS and ExoT were increased in culture medium of P. aeruginosa grown under conditions stimulatory for these toxins. The increase in ExoS was significantly correlated with reduced invasion. In vitro experiments showed that purified LasB degraded recombinant ExoS. Taken together, these studies suggest a mechanism by which invasive strains can synthesize inhibitors of invasion, ExoS and ExoT, yet still invade epithelial cells. By this mechanism, LasA and LasB decrease the levels of the toxins directly or indirectly, and thus reduce inhibition of invasion.

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Jude, Florence, Thilo Köhler, Pavel Branny, Karl Perron, Matthias P. Mayer, Rachel Comte, and Christian van Delden. "Posttranscriptional Control of Quorum-Sensing-Dependent Virulence Genes by DksA in Pseudomonas aeruginosa." Journal of Bacteriology 185, no. 12 (June 15, 2003): 3558–66. http://dx.doi.org/10.1128/jb.185.12.3558-3566.2003.

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ABSTRACT Pseudomonas aeruginosa controls the secretion of extracellular virulence factors, including rhamnolipids and LasB elastase, by the las and rhl quorum-sensing systems. Here, we mutated the dksA gene of P. aeruginosa by insertion of an Ω-Hg cassette. The mutant displayed growth rates similar to that of the wild type in rich medium but was impaired in growth in defined minimal medium. Production of rhamnolipids and LasB elastase by the dksA mutant was only 4 and 10%, respectively, of wild-type levels. These defects could be partially complemented by introduction of the plasmid-encoded dksA genes from P. aeruginosa or Escherichia coli. In the dksA mutant, the expression of rhlI was increased early during exponential growth, but expression of other quorum-sensing regulator genes—lasR, lasI, and rhlR—was not affected. Although the transcription of the lasB and rhlAB genes was comparable between the dksA mutant and the wild-type strain in peptone tryptic soy broth medium, we observed reduced translation of both genes in the dksA mutant. Similarly, we found that full translation of lasB and rhlAB genes in E. coli also requires the dksA gene. DksA is therefore a novel regulator involved in the posttranscriptional control of extracellular virulence factor production in P. aeruginosa.

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Ishida, Takenori, Tsukasa Ikeda, Noboru Takiguchi, Akio Kuroda, Hisao Ohtake, and Junichi Kato. "Inhibition of Quorum Sensing in Pseudomonas aeruginosa by N-Acyl Cyclopentylamides." Applied and Environmental Microbiology 73, no. 10 (March 16, 2007): 3183–88. http://dx.doi.org/10.1128/aem.02233-06.

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ABSTRACT N-Octanoyl cyclopentylamide (C8-CPA) was found to moderately inhibit quorum sensing in Pseudomonas aeruginosa PAO1. To obtain more powerful inhibitors, a series of structural analogs of C8-CPA were synthesized and examined for their ability to inhibit quorum sensing in P. aeruginosa PAO1. The lasB-lacZ and rhlA-lacZ reporter assays revealed that the chain length and the ring structure were critical for C8-CPA analogs to inhibit quorum sensing. N-Decanoyl cyclopentylamide (C10-CPA) was found to be the strongest inhibitor, and its concentrations required for half-maximal inhibition for lasB-lacZ and rhlA-lacZ expression were 80 and 90 μM, respectively. C10-CPA also inhibited production of virulence factors, including elastase, pyocyanin, and rhamnolipid, and biofilm formation without affecting growth of P. aeruginosa PAO1. C10-CPA inhibited induction of both lasI-lacZ by N-(3-oxododecanoyl)-l-homoserine lactone (PAI1) and rhlA-lacZ by N-butanoyl-l-homoserine lactone (PAI2) in the lasI rhlI mutant of P. aeruginosa PAO1, indicating that C10-CPA interferes with the las and rhl quorum-sensing systems via inhibiting interaction between their response regulators (LasR and RhlR) and autoinducers.

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McKnight, Susan L., Barbara H. Iglewski, and Everett C. Pesci. "The Pseudomonas Quinolone Signal Regulates rhl Quorum Sensing in Pseudomonas aeruginosa." Journal of Bacteriology 182, no. 10 (May 15, 2000): 2702–8. http://dx.doi.org/10.1128/jb.182.10.2702-2708.2000.

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ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa uses intercellular signals to control the density-dependent expression of many virulence factors. The las and rhlquorum-sensing systems function, respectively, through the autoinducersN-(3-oxododecanoyl)-l-homoserine lactone andN-butyryl-l-homoserine lactone (C4-HSL), which are known to positively regulate the transcription of the elastase-encoding gene, lasB. Recently, we reported that a second type of intercellular signal is involved in lasB induction. This signal was identified as 2-heptyl-3-hydroxy-4-quinolone and designated thePseudomonas quinolone signal (PQS). PQS was determined to be part of the quorum-sensing hierarchy since its production and bioactivity depended on the las and rhlquorum-sensing systems, respectively. In order to define the role of PQS in the P. aeruginosa quorum-sensing cascade,lacZ gene fusions were used to determine the effect of PQS on the transcription of the quorum-sensing system geneslasR, lasI, rhlR, andrhlI. We found that in P. aeruginosa, PQS caused a major induction of rhlI′-lacZ and had lesser effects on the transcription of lasR′-lacZ andrhlR′-lacZ. We also observed that the transcription of bothrhlI′-lacZ and lasB′-lacZ was cooperatively effected by C4-HSL and PQS. Additionally, we present data indicating that PQS was not produced maximally until cultures reached the late stationary phase of growth. Taken together, our results imply that PQS acts as a link between the las and rhlquorum-sensing systems and that this signal is not involved in sensing cell density.

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Cabrol, Ségolène, Anne Olliver, Gerald B. Pier, Antoine Andremont, and Raymond Ruimy. "Transcription of Quorum-Sensing System Genes inClinical and Environmental Isolates of Pseudomonasaeruginosa." Journal of Bacteriology 185, no. 24 (December 15, 2003): 7222–30. http://dx.doi.org/10.1128/jb.185.24.7222-7230.2003.

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ABSTRACT Quorum sensing (QS)-based transcriptional responses in Pseudomonas aeruginosa have been defined on the basis of increases in transcript levels of QS-controlled genes such as lasB and aprA following the hierarchical transcriptional increases of central controllers such as the lasR gene. These increases occur at high bacterial concentrations such as early-stationary-phase growth in vitro. However, the extent to which the increases occur in a variety of clinical and environmental isolates has not been determined nor is there extensive information on allelic variation in lasR genes. An analysis of the sequences of the lasR gene among 66 clinical and environmental isolates showed that 81% have a sequence either identical to that of strain PAO1 or with a silent mutation, 15% have nucleotide changes resulting in amino acid changes, and 5% have an insertion sequence in the lasR gene. Using real-time PCR to quantify transcript levels of lasR, lasB, and aprA in the early log and early stationary phases among 35 isolates from bacteremia and pneumonia cases and the environment, we found most (33 of 35) strains had increases in lasR transcripts in early stationary phase but with a very wide range of final transcript levels per cell. There was a strong correlation (r 2 = 0.84) between early-log- and early-stationary-phase transcript levels in all strains, but this finding remained true only for the 50% of strains above the median level of lasR found in early log phase. There were significant (P < 0.05) but weak-to-modest correlations of lasR transcript levels with aprA (r2= 0.2) and lasB (r 2 = 0.5) transcript levels, but again this correlation occurred only in the 50% of P. aeruginosa strains with the highest levels of lasR transcripts in early stationary phase. There were no differences in distribution of lasR alleles among the bacteremia, pneumonia, or environmental isolates. Overall, only about 50% of P. aeruginosa strains from clinical and environmental sources show a lasR-dependent increase in the transcription of aprA and lasB genes, indicating that for about 50% of clinical isolates this regulatory system may not play a significant role in pathogenesis.

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Zhao, Chaoyue, Hongda Zheng, Liman Zhou, Hongrui Ji, Lu Zhao, Wengong Yu, and Qianhong Gong. "Falcarindiol Isolated from Notopterygium incisum Inhibits the Quorum Sensing of Pseudomonas aeruginosa." Molecules 26, no. 19 (September 29, 2021): 5896. http://dx.doi.org/10.3390/molecules26195896.

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Quorum sensing (QS) is employed by the opportunistic pathogen Pseudomonas aeruginosa to regulate physiological behaviors and virulence. QS inhibitors (QSIs) are potential anti-virulence agents for the therapy of P. aeruginosa infection. During the screening for QSIs from Chinese herbal medicines, falcarindiol (the major constituent of Notopterygium incisum) exhibited QS inhibitory activity. The subinhibitory concentration of falcarindiol exerted significant inhibitory effects on the formation of biofilm and the production of virulence factors such as elastase, pyocyanin, and rhamnolipid. The mRNA expression of QS-related genes (lasB, phzH, rhlA, lasI, rhlI, pqsA, and rhlR) was downregulated by falcarindiol while that of lasR was not affected by falcarindiol. The transcriptional activation of the lasI promoter was inhibited by falcarindiol in the P. aeruginosa QSIS-lasI selector. Further experiments confirmed that falcarindiol inhibited the las system using the reporter strain Escherichia coli MG4/pKDT17. Electrophoretic mobility shift assay (EMSA) showed that falcarindiol inhibited the binding of the transcription factor LasR and the lasI promoter region. Molecular docking showed that falcarindiol interacted with the Tyr47 residue, leading to LasR instability. The decrease of LasR-mediated transcriptional activation was responsible for the reduction of downstream gene expression, which further inhibited virulence production. The inhibition mechanism of falcarindiol to LasR provides a theoretical basis for its medicinal application.

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Hamood, Abdul N., and John Griswold. "DNA hybridization analysis of thePseudomonas aeruginosaelastase gene [lasB) from different clinical isolates." Canadian Journal of Microbiology 41, no. 10 (October 1, 1995): 910–17. http://dx.doi.org/10.1139/m95-125.

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Pseudomonas aeruginosa produces several extracellular virulence factors including elastase (which is encoded by lasB). Recently, we examined several clinical isolates of P. aeruginosa for the production of toxin A, elastase, exoenzyme S, and phospholipase C. Although the majority of the isolates produced a high level of elastase, a few isolates produced either very low or no detectable elastase. In this study, we tried to determine the presence of restriction site heterogeneity within lasB from these isolates and the possible correlation between such heterogeneity and the observed variation in elastase production. Chromosomal DNA from the isolates was digested with different restriction enzymes and examined by Southern blot hybridization experiments using two lasB probes. One lasB probe covers 636 bp of lasB structural gene while the other covers 240 bp of the lasB upstream region. Chromosomal DNA from P. aeruginosa PAO1 and PA103 was used as controls. Results indicate that chromosomal DNA from all isolates hybridized to both lasB probes. Depending on the restriction enzyme used for DNA digestion, lasB from 3 to 12% of the isolates showed different patterns of hybridization with the lasB structural gene probe. However, no difference in the hybridization pattern was seen with the lasB upstream probe. With the exception of one isolate, hybridization of genomic DNA from different isolates (with both probes) produced a single hybridization band. In that isolate, an additional hybridization band was detected. Immunoblotting experiments confirmed that elastase protein is not produced by 6 out of 67 isolates. However, lasB from four of these elastase-deficient strains showed no difference in the hybridization pattern with either lasB probe. These results suggest that (i) lasB is present as a single copy in all but one isolate; (ii) with the exception of one, the lasB upstream region from different P. aeruginosa isolates contains no restriction site polymorphism; (iii) the observed heterogeneity within lasB structural genes is limited; and (iv) variations in the hybridization patterns of lasB from different isolates do not correlate with the differences between these isolates in elastase production.Key words: Pseudomonas aeruginosa, clinical isolates, DNA hybridization, elastase, lasB.

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O. M. Al-Dahmoshi, Hussein, Noor S. Al-Khafaji, Ahmed Abdulzahra Jeyad, Hasanain Khaleel Shareef, and Rafah F. Al-Jebori. "Molecular Detection of Some Virulence Traits among Pseudomonas aeruginosa Isolates, Hilla-Iraq." Biomedical and Pharmacology Journal 11, no. 2 (May 24, 2018): 835–42. http://dx.doi.org/10.13005/bpj/1439.

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Wound infections regards one of the most common infections encountered in hospital records. Pseudomonas aeruginosa regard the 3rd common pathogen among healthcare-related infections. Their ability to adapt to different conditions and presence of pool of virulence factors may render their infections delay in healing. During a period of six months 114 wound swabs were collected and inoculated on Pseudomonas chromogenic agar and then Pseudomonas aeruginosa isolated confirmed by PCR using specific primer for 16S rDNA gene of Pseudomonas aeruginosa. Molecular investigation of some virulence factor like ExoA, OprL, OprI, LasI and LasB were performed using a sets of specific primer pairs. The results revealed that only 26 (22.8%) isolates were Pseudomonas aeruginosa and the coexistence of more than one virulence factors within the same isolates was also recorder. OprI and LasB were most common followed by LasI, ExoA and OprL. Occurrence of virulence factor genes were 12(46.15%) for exoA, oprL was 11(42.3%), oprI was 22(84.61%), lasI was 14(53.84%) and lasB was 18(69.23%). Results of this study can lead us to conclude that P. aeruginosa have an arrays of virulence traits via which can adapt to different conditions and so cause a wide-ranging of hard to cured infections and the delay in healing and worseness degree may be attributed to owning multivirulence factors.

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Yu, Hua, Xiaomei He, Wei Xie, Junzhi Xiong, Halei Sheng, Shaodong Guo, Chunji Huang, Di Zhang, and Kebin Zhang. "Elastase LasB of Pseudomonas aeruginosa promotes biofilm formation partly through rhamnolipid-mediated regulation." Canadian Journal of Microbiology 60, no. 4 (April 2014): 227–35. http://dx.doi.org/10.1139/cjm-2013-0667.

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Elastase LasB, an important extracellular virulence factor, is shown to play an important role in the pathogenicity of Pseudomonas aeruginosa during host infection. However, the role of LasB in the life cycle of P. aeruginosa is not completely understood. This report focuses on the impact of LasB on biofilm formation of P. aeruginosa PAO1. Here, we reported that the lasB deletion mutant (ΔlasB) displayed significantly decreased bacterial attachment, microcolony formation, and extracellular matrix linkage in biofilm associated with decreased biosynthesis of rhamnolipids compared with PAO1 and lasB complementary strain (ΔlasB+). Nevertheless, the ΔlasB developed restored biofilm formation with supplementation of exogenous rhamnolipids. Further gene expression analysis revealed that the mutant of lasB could result in the downregulation of rhamnolipid synthesis at the transcriptional level. Taken together, these results indicated that LasB could promote biofilm formation partly through the rhamnolipid-mediated regulation.

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Kiratisin, Pattarachai, Kenneth D. Tucker, and Luciano Passador. "LasR, a Transcriptional Activator of Pseudomonas aeruginosa Virulence Genes, Functions as a Multimer." Journal of Bacteriology 184, no. 17 (September 1, 2002): 4912–19. http://dx.doi.org/10.1128/jb.184.17.4912-4919.2002.

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ABSTRACT The Pseudomonas aeruginosa LasR protein functions in concert with N-3-oxo-dodecanoyl-l-homoserine lactone (3O-C12-HSL) to coordinate the expression of target genes, including many genes that encode virulence factors, with cell density. We used a LexA-based protein interaction assay to demonstrate that LasR forms multimers only when 3O-C12-HSL is present. A series of LasR molecules containing internal deletions or substitutions in single, conserved amino acid residues indicated that the N-terminal portion of LasR is required for multimerization. Studies performed with these mutant versions of LasR demonstrated that the ability of LasR to multimerize correlates with its ability to function as a transcriptional activator of lasI, a gene known to be tightly regulated by the LasR-3O-C12-HSL regulatory system. A LasR molecule that carries a C-terminal deletion can function as a dominant-negative mutant in P. aeruginosa, as shown by its ability to decrease expression of lasB, another LasR-3O-C12-HSL target gene. Taken together, our data strongly support the hypothesis that LasR functions as a multimer in vivo.

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Diggle, Stephen P., Klaus Winzer, Andrée Lazdunski, Paul Williams, and Miguel Cámara. "Advancing the Quorum in Pseudomonas aeruginosa: MvaT and the Regulation of N-Acylhomoserine Lactone Production and Virulence Gene Expression." Journal of Bacteriology 184, no. 10 (May 15, 2002): 2576–86. http://dx.doi.org/10.1128/jb.184.10.2576-2586.2002.

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ABSTRACT Pseudomonas aeruginosa regulates the production of many exoproteins and secondary metabolites via a hierarchical quorum-sensing cascade through LasR and RhlR and their cognate signal molecules N-(3-oxododecanoyl)-l-homoserine lactone (3O-C12-HSL) and N-(butanoyl)-l-homoserine lactone (C4-HSL). In this study, we found that transcription of the quorum sensing-regulated genes lecA (coding for PA-IL lectin), lasB (coding for elastase), and rpoS appeared to be growth phase dependent and their expression could not be advanced to the logarithmic phase in cells growing in batch culture by the addition of exogenous C4-HSL and 3O-C12-HSL. To identify novel regulators responsible for this growth phase dependency, a P. aeruginosa lecA::lux reporter strain was subjected to random transposon mutagenesis. A number of mutants affected in lecA expression were found that exhibited altered production of multiple quorum sensing-dependent phenotypes. While some mutations were mapped to new loci such as clpA and mvaT and a putative efflux system, a number of mutations were also mapped to known regulators such as lasR, rhlR, and rpoS. MvaT was identified as a novel global regulator of virulence gene expression, as a mutation in mvaT resulted in enhanced lecA expression and pyocyanin production. This mutant also showed altered swarming ability and production of the LasB and LasA proteases, 3O-C12-HSL, and C4-HSL. Furthermore, addition of exogenous 3O-C12-HSL and C4-HSL to the mvaT mutant significantly advanced lecA expression, suggesting that MvaT is involved in the growth phase-dependent regulation of the lecA gene.

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Michel, Gérard, Geneviève Ball, Joanna B. Goldberg, and Andrée Lazdunski. "Alteration of the Lipopolysaccharide Structure Affects the Functioning of the Xcp Secretory System inPseudomonas aeruginosa." Journal of Bacteriology 182, no. 3 (February 1, 2000): 696–703. http://dx.doi.org/10.1128/jb.182.3.696-703.2000.

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ABSTRACT Pseudomonas aeruginosa secretes a wide range of hydrolytic enzymes into the external medium by the Xcp secretion machinery. To better understand the role played by envelope constituents in the functioning of this type II secretory system, we have studied the influence of lipopolysaccharide (LPS) on the secretion of two extracellular enzymes, the elastase LasB and the lipase LipA. Strains with defective LPS decreased production of LasB and altered the secretion processes of both LasB and LipA without any apparent effect on the composition of the Xcp machinery. The PAO1algCstrain, defective in the outer core of LPS, was leaky, as shown by the extracellular release of the periplasmic β-lactamase. Generation of an xcpR mutation in this mutant led only to a partial accumulation of LasB within the cells, indicating that in strain PAO1algC with a functional xcpR gene, LasB was released in the extracellular medium partly by leakage and partly by secretion. The pool of LasB released into the medium by leakage was not recovered in an active form, while extracellular LasB was active when secreted via the secretory machinery. Further analysis revealed that the presence of a functional Xcp machinery is strictly required for the activation process of LasB. Our results provide evidence that the Xcp system is not fully functional when the LPS structure of P. aeruginosa is altered.

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Santajit, Sirijan, Thida Kong-ngoen, Manas Chongsa-Nguan, Usa Boonyuen, Pornpan Pumirat, Nitat Sookrung, Wanpen Chaicumpa, and Nitaya Indrawattana. "Human Single-Chain Antibodies That Neutralize Elastolytic Activity of Pseudomonas aeruginosa LasB." Pathogens 10, no. 6 (June 17, 2021): 765. http://dx.doi.org/10.3390/pathogens10060765.

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LasB (elastase/pseudolysin) is an injurious zinc-metalloprotease secreted by the infecting Pseudomonas aeruginosa. LasB is recognized as the bacterial key virulence factor for establishment of successful infection, acquisition of nutrients, dissemination, tissue invasion, and immune modulation and evasion. LasB digests a variety of the host tissue proteins, extracellular matrices, as well as components of both innate and adaptive immune systems, including immunoglobulins, complement proteins, and cytokines. Thus, this enzyme is an attractive target for disarming the P. aeruginosa. This study generated human single-chain antibodies (HuscFvs) that can neutralize the elastolytic activity of native LasB by using phage display technology. Gene sequences coding HuscFvs (huscfvs) isolated from HuscFv-displaying phage clones that bound to enzymatically active LasB were sub-cloned to expression plasmids for large scale production of the recombinant HuscFvs by the huscfv-plasmid transformed Escherichia coli. HuscFvs of two transformed E. coli clones, i.e., HuscFv-N42 and HuscFv-N45, neutralized the LasB elastolytic activities in vitro. Computer simulation by homology modeling and molecular docking demonstrated that antibodies presumptively formed contact interfaces with the LasB residues critical for the catalytic activity. Although the LasB neutralizing mechanisms await elucidation by laboratory experiments, the HuscFvs should be tested further towards the clinical application as a novel adjunctive therapeutics to mitigate severity of the diseases caused by P. aeruginosa.

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Vandeputte, Olivier M., Martin Kiendrebeogo, Tsiry Rasamiravaka, Caroline Stévigny, Pierre Duez, Sanda Rajaonson, Billo Diallo, Adeline Mol, Marie Baucher, and Mondher El Jaziri. "The flavanone naringenin reduces the production of quorum sensing-controlled virulence factors in Pseudomonas aeruginosa PAO1." Microbiology 157, no. 7 (July 1, 2011): 2120–32. http://dx.doi.org/10.1099/mic.0.049338-0.

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Preliminary screening of the Malagasy plant Combretum albiflorum for compounds attenuating the production of quorum sensing (QS)-controlled virulence factors in bacteria led to the identification of active fractions containing flavonoids. In the present study, several flavonoids belonging to the flavone, flavanone, flavonol and chalcone structural groups were screened for their capacity to reduce the production of QS-controlled factors in the opportunistic pathogen Pseudomonas aeruginosa (strain PAO1). Flavanones (i.e. naringenin, eriodictyol and taxifolin) significantly reduced the production of pyocyanin and elastase in P. aeruginosa without affecting bacterial growth. Consistently, naringenin and taxifolin reduced the expression of several QS-controlled genes (i.e. lasI, lasR, rhlI, rhlR, lasA, lasB, phzA1 and rhlA) in P. aeruginosa PAO1. Naringenin also dramatically reduced the production of the acylhomoserine lactones N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C12-HSL) and N-butanoyl-l-homoserine lactone (C4-HSL), which is driven by the lasI and rhlI gene products, respectively. In addition, using mutant strains deficient for autoinduction (ΔlasI and ΔrhlI) and LasR- and RhlR-based biosensors, it was shown that QS inhibition by naringenin not only is the consequence of a reduced production of autoinduction compounds but also results from a defect in the proper functioning of the RlhR–C4-HSL complex. Widely distributed in the plant kingdom, flavonoids are known for their numerous and determinant roles in plant physiology, plant development and in the success of plant–rhizobia interactions, but, as shown here, some of them also have a role as inhibitors of the virulence of pathogenic bacteria by interfering with QS mechanisms.

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Branny, Pavel, James P. Pearson, Everett C. Pesci, Thilo Köhler, Barbara H. Iglewski, and Christian Van Delden. "Inhibition of Quorum Sensing by a Pseudomonas aeruginosa dksA Homologue." Journal of Bacteriology 183, no. 5 (March 1, 2001): 1531–39. http://dx.doi.org/10.1128/jb.183.5.1531-1539.2001.

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ABSTRACT The Pseudomonas aeruginosa las (lasR-lasI) andrhl (rhlR-rhlI) quorum-sensing systems regulate the expression of several virulence factors, including elastase and rhamnolipid. P. aeruginosa strain PR1-E4 is alasR deletion mutant that contains a second, undefined mutation which allows production of elastase and rhamnolipid despite a nonfunctional las system. We have previously shown that this strain accomplishes this by increasing the expression of the autoinducer synthase gene rhlI. In this report, we show that the elastolytic phenotype of mutant PR1-E4 can be complemented with a P. aeruginosa homologue of the Escherichia coli dnaK mutation suppressor gene dksA. When supplied in trans on a multicopy plasmid, this gene completely suppressed elastase production by mutant PR1-E4. Cloning and Northern blot analysis revealed that dksA was neither mutated nor less transcribed in mutant PR1-E4. When overexpressed,dksA also reduced rhamnolipid production by both mutant PR1-E4 and the wild type, PAO1. Using Northern blot analysis andlacZ reporter fusions, we show that dksAinhibits rhlI, rhlAB, and lasB transcription. Exogenous N-butyryl–l-homoserine lactone overcame the reduced expression of rhlI and restoredrhlAB and lasB expression, as well as elastase production. Our results suggest that the overproduction of the P. aeruginosa DksA homologue inhibits quorum-sensing-dependent virulence factor production by downregulating the transcription of the autoinducer synthase gene rhlI.

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Velázquez-Libera, José Luis, Juliana Andrea Murillo-López, Alexander F. de la Torre, and Julio Caballero. "Structural Requirements of N-alpha-Mercaptoacetyl Dipeptide (NAMdP) Inhibitors of Pseudomonas Aeruginosa Virulence Factor LasB: 3D-QSAR, Molecular Docking, and Interaction Fingerprint Studies." International Journal of Molecular Sciences 20, no. 24 (December 5, 2019): 6133. http://dx.doi.org/10.3390/ijms20246133.

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The zinc metallopeptidase Pseudomonas elastase (LasB) is a virulence factor of Pseudomonas aeruginosa (P. aeruginosa), a pathogenic bacterium that can cause nosocomial infections. The present study relates the structural analysis of 118 N-alpha-mercaptoacetyl dipeptides (NAMdPs) as LasB inhibitors. Field-based 3D-QSAR and molecular docking methods were employed to describe the essential interactions between NAMdPs and LasB binding sites, and the chemical features that determine their differential activities. We report a predictive 3D-QSAR model that was developed according to the internal and external validation tests. The best model, including steric, electrostatic, hydrogen bond donor, hydrogen bond acceptor, and hydrophobic fields, was found to depict a three-dimensional map with the local positive and negative effects of these chemotypes on the LasB inhibitory activities. Furthermore, molecular docking experiments yielded bioactive conformations of NAMdPs inside the LasB binding site. The series of NAMdPs adopted a similar orientation with respect to phosphoramidon within the LasB binding site (crystallographic reference), where the backbone atoms of NAMdPs are hydrogen-bonded to the LasB residues N112, A113, and R198, similarly to phosphoramidon. Our study also included a deep description of the residues involved in the protein–ligand interaction patterns for the whole set of NAMdPs, through the use of interaction fingerprints (IFPs).

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Leduc, Dominique, Nathalie Beaufort, Sophie de Bentzmann, Jean-Claude Rousselle, Abdelkader Namane, Michel Chignard, and Dominique Pidard. "The Pseudomonas aeruginosa LasB Metalloproteinase Regulates the Human Urokinase-Type Plasminogen Activator Receptor through Domain-Specific Endoproteolysis." Infection and Immunity 75, no. 8 (May 21, 2007): 3848–58. http://dx.doi.org/10.1128/iai.00015-07.

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ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen in human lungs, where its secretable LasB metalloproteinase can be a virulence factor. The urokinase-type plasminogen activator receptor (uPAR) participates in pericellular proteolysis and the adherence/migration of epithelial cells and leukocytes recruited during infection and shows functional regulation by various proteinases via limited endoproteolysis occurring within its three domains (D1 to D3). We thus examined the proteolytic activity of LasB on uPAR by using recombinant uPAR as well as uPAR-expressing, human monocytic, and bronchial epithelial cell lines. Protein immunoblotting and flow immunocytometry using a panel of domain-specific anti-uPAR antibodies showed that LasB is able to cleave uPAR both within the sequence linking D1 to D2 and at the carboxy terminus of D3. Comparison of LasB-producing and LasB-deficient bacterial strains indicated that LasB is entirely responsible for the uPAR cleavage ability of P. aeruginosa. Based on amino-terminal protein microsequencing and mass spectrometry analysis of the cleavage of peptides mimicking the uPAR sequences targeted by LasB, cleavage sites were determined to be Ala84-Val85 and Thr86-Tyr87 (D1-D2) and Gln279-Tyr280 (D3). Such a dual cleavage of uPAR led to the removal of amino-terminal D1, the generation of a truncated D2D3 species, and the shedding of D2D3 from cells. This proteolytic processing of uPAR was found to (i) drastically reduce the capacity of cells to bind urokinase and (ii) abrogate the interaction between uPAR and the matrix adhesive protein vitronectin. The LasB proteinase is thus endowed with a high potential for the alteration of uPAR expression and functioning on inflammatory cells during infections by P. aeruginosa.

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Cathcart, George R. A., Derek Quinn, Brett Greer, Pat Harriott, John F. Lynas, Brendan F. Gilmore, and Brian Walker. "Novel Inhibitors of the Pseudomonas aeruginosa Virulence Factor LasB: a Potential Therapeutic Approach for the Attenuation of Virulence Mechanisms in Pseudomonal Infection." Antimicrobial Agents and Chemotherapy 55, no. 6 (March 28, 2011): 2670–78. http://dx.doi.org/10.1128/aac.00776-10.

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ABSTRACTPseudomonas elastase (LasB), a metalloprotease virulence factor, is known to play a pivotal role in pseudomonal infection. LasB is secreted at the site of infection, where it exerts a proteolytic action that spans from broad tissue destruction to subtle action on components of the host immune system. The former enhances invasiveness by liberating nutrients for continued growth, while the latter exerts an immunomodulatory effect, manipulating the normal immune response. In addition to the extracellular effects of secreted LasB, it also acts within the bacterial cell to trigger the intracellular pathway that initiates growth as a bacterial biofilm. The key role of LasB in pseudomonal virulence makes it a potential target for the development of an inhibitor as an antimicrobial agent. The concept of inhibition of virulence is a recently established antimicrobial strategy, and such agents have been termed “second-generation” antibiotics. This approach holds promise in that it seeks to attenuate virulence processes without bactericidal action and, hence, without selection pressure for the emergence of resistant strains. A potent inhibitor of LasB,N-mercaptoacetyl-Phe-Tyr-amide (Ki= 41 nM) has been developed, and its ability to block these virulence processes has been assessed. It has been demonstrated that thes compound can completely block the action of LasB on protein targets that are instrumental in biofilm formation and immunomodulation. The novel LasB inhibitor has also been employed in bacterial-cell-based assays, to reduce the growth of pseudomonal biofilms, and to eradicate biofilm completely when used in combination with conventional antibiotics.

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Saint-Criq, Vinciane, Bérengère Villeret, Fabien Bastaert, Saadé Kheir, Aurélie Hatton, Aurélie Cazes, Zhou Xing, et al. "Pseudomonas aeruginosa LasB protease impairs innate immunity in mice and humans by targeting a lung epithelial cystic fibrosis transmembrane regulator–IL-6–antimicrobial–repair pathway." Thorax 73, no. 1 (August 8, 2017): 49–61. http://dx.doi.org/10.1136/thoraxjnl-2017-210298.

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BackgroundPseudomonas aeruginosa lung infections are a huge problem in ventilator-associated pneumonia, cystic fibrosis (CF) and in chronic obstructive pulmonary disease (COPD) exacerbations. This bacterium secretes virulence factors that may subvert host innate immunity.ObjectiveWe evaluated the effect of P. aeruginosa elastase LasB, an important virulence factor secreted by the type II secretion system, on ion transport, innate immune responses and epithelial repair, both in vitro and in vivo.MethodsWild-type (WT) or cystic fibrosis transmembrane conductance regulator (CFTR)-mutated epithelial cells (cell lines and primary cells from patients) were treated with WT or ΔLasB pseudomonas aeruginosa O1 (PAO1) secretomes. The effect of LasB and PAO1 infection was also assessed in vivo in murine models.ResultsWe showed that LasB was the most abundant protein in WT PAO1 secretomes and that it decreased epithelial CFTR expression and activity. In airway epithelial cell lines and primary bronchial epithelial cells, LasB degraded the immune mediators interleukin (IL)-6 and trappin-2, an important epithelial-derived antimicrobial molecule. We further showed that an IL-6/STAT3 signalling pathway was downregulated by LasB, resulting in inhibition of epithelial cell repair. In mice, intranasally instillated LasB induced significant weight loss, inflammation, injury and death. By contrast, we showed that overexpression of IL-6 and trappin-2 protected mice against WT-PAO1-induced death, by upregulating IL-17/IL-22 antimicrobial and repair pathways.ConclusionsOur data demonstrate that PAO1 LasB is a major P. aeruginosa secreted factor that modulates ion transport, immune response and tissue repair. Targeting this virulence factor or upregulating protective factors such as IL-6 or antimicrobial molecules such as trappin-2 could be beneficial in P. aeruginosa-infected individuals.

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Yoshida, Makoto, Keiichi Koyama, Takuo Sakon, Akira Ochiai, and Mitsuhiro Motokawa. "Cyclotron Resonance of LaSb." Journal of the Physical Society of Japan 69, no. 11 (November 15, 2000): 3629–32. http://dx.doi.org/10.1143/jpsj.69.3629.

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van Delden, Christian, Rachel Comte, and And Marc Bally. "Stringent Response Activates Quorum Sensing and Modulates Cell Density-Dependent Gene Expression inPseudomonas aeruginosa." Journal of Bacteriology 183, no. 18 (September 15, 2001): 5376–84. http://dx.doi.org/10.1128/jb.183.18.5376-5384.2001.

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ABSTRACT During nutrient starvation, Escherichia coli elicits a stringent response involving the ribosome-associated protein RelA. Activation of RelA results in a global change in the cellular metabolism including enhanced expression of the stationary-phase sigma factor RpoS. In the human pathogen Pseudomonas aeruginosa, a complex quorum-sensing circuitry, linked to RpoS expression, is required for cell density-dependent production of many secreted virulence factors, including LasB elastase. Quorum sensing relies on the activation of specific transcriptional regulators (LasR and RhlR) by their corresponding autoinducers (3-oxo-C12-homoserine lactone [HSL] and C4-HSL), which function as intercellular signals. We found that overexpression of relA activated the expression of rpoS in P. aeruginosa and led to premature, cell density-independent LasB elastase production. We therefore investigated the effects of the stringent response on quorum sensing. Both lasR and rhlR gene expression and autoinducer synthesis were prematurely activated during the stringent response induced by overexpression of relA. Premature expression of lasR and rhlR was also observed when relA was overexpressed in a PAO1 rpoSmutant. The stringent response induced by the amino acid analogue serine hydroxamate (SHX) also led to premature production of the 3-oxo-C12-HSL autoinducer. This response to SHX was absent in a PAO1 relA mutant. These findings suggest that the stringent response can activate the two quorum-sensing systems of P. aeruginosa independently of cell density.

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Alasil, Saad Musbah, Rahmat Omar, Salmah Ismail, and Mohd Yasim Yusof. "Inhibition of Quorum Sensing-Controlled Virulence Factors and Biofilm Formation in Pseudomonas aeruginosa by Culture Extract from Novel Bacterial Species of Paenibacillus Using a Rat Model of Chronic Lung Infection." International Journal of Bacteriology 2015 (January 11, 2015): 1–16. http://dx.doi.org/10.1155/2015/671562.

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Quorum sensing (QS) is a key regulator of virulence factors and biofilm formation in Gram-negative bacteria such as Pseudomonas aeruginosa. Microorganisms that inhabit soil are of strategic importance in the discovery of compounds with anti-QS properties. The objective of the study was to test the culture extract of a taxonomically novel species of Paenibacillus strain 139SI for its inhibitory effects on the QS-controlled virulence factors and biofilm formation of Pseudomonas aeruginosa both in vitro and in vivo. The Paenibacillus sp. culture extract was used to test its anti-QS effects on the LasA protease, LasB elastase, pyoverdin production, and biofilm formation of P. aeruginosa as well as evaluate its therapeutic effects on lung bacteriology, pathology, hematological profile, and serum antibody responses of experimental animals in a rat model of chronic lung infection. Results showed significant decrease in the activities of QS-controlled LasA protease, LasB elastase pyoverdin, and biofilm formation of P. aeruginosa caused by the culture extract. Moreover, the extract significantly prolonged the survival times of rats and facilitated the clearance of biofilm infections from infected lungs. In conclusion, the antiquorum sensing effects of culture extract from a novel species of Paenibacillus provide new insights to combat biofilm-associated infections.

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Wang, Mengjia, Lu Zhao, Hao Wu, Chaoyue Zhao, Qianhong Gong, and Wengong Yu. "Cladodionen Is a Potential Quorum Sensing Inhibitor Against Pseudomonas aeruginosa." Marine Drugs 18, no. 4 (April 10, 2020): 205. http://dx.doi.org/10.3390/md18040205.

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Pseudomonas aeruginosa is an opportunistic pathogen using virulence factors and biofilm regulated by quorum sensing (QS) systems to infect patients and protect itself from environmental stress and antibiotics. Interfering with QS systems is a novel approach to combat P. aeruginosa infections without killing the bacteria, meaning that it is much harder for bacteria to develop drug resistance. A marine fungus Cladosporium sp. Z148 with anti-QS activity was obtained from Jiaozhou Bay, China. Cladodionen, a novel QS inhibitor, was isolated from the extracts of this fungus. Cladodionen had a better inhibitory effect than pyocyanin on the production of elastase and rhamnolipid. It also inhibited biofilm formation and motilities. The mRNA expressions of QS-related genes, including receptor proteins (lasR, rhlR and pqsR), autoinducer synthases (lasI, rhlI and pqsA) and virulence factors (lasB and rhlA) were down-regulated by cladodionen. Molecular docking analysis showed that cladodionen had better binding affinity to LasR and PqsR than natural ligands. Moreover, the binding affinity of cladodionen to LasR was higher than to PqsR. Cladodionen exhibits potential as a QS inhibitor against P. aeruginosa, and its structure–activity relationships should be further studied to illustrate the mode of action, optimize its structure and improve anti-QS activity.

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Fiebig, David, Anita Anderl, Sahra Al Djaizani, Harald Kolmar, and Hans-Lothar Fuchsbauer. "Dissecting capture and twisting of aureolysin and pseudolysin: functional amino acids of the Dispase autolysis-inducing protein." Biochemical Journal 477, no. 13 (July 17, 2020): 2595–606. http://dx.doi.org/10.1042/bcj20200407.

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The Dispase autolysis-inducing protein (DAIP) from Streptomyces mobaraensis attracts M4 metalloproteases, which results in inhibition and autolysis of bacillolysin (BL) and thermolysin (TL). The present study shows that aureolysin (AL) from Staphylococcus aureus and pseudolysin (LasB) from Pseudomonas aeruginosa are likewise impaired by DAIP. Complete inhibition occurred when DAIP significantly exceeded the amount of the target protease. At low DAIP concentrations, AL and BL performed autolysis, while LasB and TL degradation required reductants or detergents that break intramolecular disulfide bonds or change the protein structure. Site directed mutagenesis of DAIP and removal of an exposed protein loop either influenced binding or inhibition of AL and TL but had no effect on LasB and BL. The Y170A and Δ239–248 variants had completely lost affinity for TL and AL. The exchange of Asn-275 also impaired the interaction of DAIP with AL. In contrast, DAIP Phe-297 substitution abolished inhibition and autolysis of both target proteases but still allowed complex formation. Our results give rise to the conclusion that other, yet unknown DAIP amino acids inactivate LasB and BL. Obviously, various bacteria in the same habitat caused Streptomyces mobaraensis to continuously optimize DAIP in inactivating the tackling metalloproteases.

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Beaufort, Nathalie, Paulina Seweryn, Sophie de Bentzmann, Aihua Tang, Josef Kellermann, Nicolai Grebenchtchikov, Manfred Schmitt, Christian P. Sommerhoff, Dominique Pidard, and Viktor Magdolen. "Activation of human pro-urokinase by unrelated proteases secreted by Pseudomonas aeruginosa." Biochemical Journal 428, no. 3 (May 27, 2010): 473–82. http://dx.doi.org/10.1042/bj20091806.

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Pathogenic bacteria, including Pseudomonas aeruginosa, interact with and engage the host plasminogen (Plg) activation system, which encompasses the urokinase (uPA)-type Plg activator, and is involved in extracellular proteolysis, including matrilysis and fibrinolysis. We hypothesized that secreted bacterial proteases might contribute to the activation of this major extracellular proteolytic system, thereby participating in bacterial dissemination. We report that LasB, a thermolysin-like metalloprotease secreted by Ps. aeruginosa, converts the human uPA zymogen into its active form (kcat=4.9 s−1, Km=8.9 μM). Accordingly, whereas the extracellular secretome from the LasB-expressing pseudomonal strain PAO1 efficiently activates pro-uPA, the secretome from the isogenic LasB-deficient strain PDO240 is markedly less potent in pro-uPA activation. Still, both secretomes induce some metalloprotease-independent activation of the human zymogen. The latter involves a serine protease, which we identified via both recombinant protein expression in Escherichia coli and purification from pseudomonal cultures as protease IV (PIV; kcat=0.73 s−1, Km=6.2 μM). In contrast, neither secretomes nor the pure proteases activate Plg. Along with this, LasB converts Plg into mini-Plg and angiostatin, whereas, as reported previously, it processes the uPA receptor, inactivates the plasminogen activator inhibitor 1, and activates pro-matrix metalloproteinase 2. PIV does not target these factors at all. To conclude, LasB and PIV, although belonging to different protease families and displaying quite different substrate specificities, both activate the urokinase-type precursor of the Plg activation cascade. Direct pro-uPA activation, as also reported for other bacterial proteases, might be a frequent phenomenon that contributes to bacterial virulence.

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Raja, Srinivasa N., Rolf-Detlef Treede, and David S. Warner. "Testing the Link between Sympathetic Efferent and Sensory Afferent Fibers in Neuropathic Pain." Anesthesiology 117, no. 1 (July 1, 2012): 173–77. http://dx.doi.org/10.1097/aln.0b013e31825adb2b.

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The diagnosis of sympathetically maintained pain (SMP) is typically established by assessment of pain relief during local anesthetic blockade of the sympathetic ganglia that innervate the painful body part. To determine if systemic α-adrenergic blockade with phentolamine can be used to diagnose SMP, we compared the effects on pain of local anesthetic sympathetic ganglion blocks (LASB) and phentolamine blocks (PhB) in 20 patients with chronic pain and hyperalgesia that were suspected to be sympathetically maintained. The blocks were done inrandom order on separate days. Patients rated the intensity of ongoing and stimulus-evoked pain every 5 min before, during, and after the LASB and PhB. Patients and the investigator assessing pain levels were blinded to the time of intravenous administration of phentolamine (total dose 25-35 mg). The pain relief achieved by LASB and PhB correlated closely (r = 0.84), and there was no significant difference in the maximum pain relief achieved with the two blocks (t = 0.19, P > 0.8). Nine patients experienced a greater than 50% relief of pain and hyperalgesia from both LASB and PhB and were considered to have a clinically significant component of SMP. We conclude that α-adrenergic blockade with intravenous phentolamine is a sensitive alternative test to identify patients with SMP.

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Silva, Stephanie Targino, Jailton Lobo da Costa Lima, Marcelle Aquino Rabelo, Armando Monteiro Bezerra Neto, Lílian Rodrigues Alves, Jussyêgles Niedja da Paz Pereira, Ana Catarina de Souza Lopes, and Maria Amélia Vieira Maciel. "Phenotypic and genetic analysis of virulence factors in multidrug- sensitive and multidrug-resistant clinical isolates of Pseudomonas aeruginosa." Research, Society and Development 10, no. 11 (September 6, 2021): e457101120032. http://dx.doi.org/10.33448/rsd-v10i11.20032.

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This study aimed to correlate the pattern of antimicrobial susceptibility, phenotypic production of virulence factors, the occurrence of virulence factors genes and the clonal profile of clinical isolates of Pseudomonas aeruginosa of a tertiary hospital in Recife-PE. The 30 clinical isolates (15 multidrug-sensitive (MDS) and 15 multidrug-resistant (MDR)) were analyzed using phenotypic methods to detect virulence factors (alkaline protease, hemolysin, phospholipase C, lipase, and pigments). The detection of the aprA, lasA, lasB, plcH, and toxA genes was performed through specific PCRs, and the clonal profile was assessed using ERIC-PCR. The results revealed cephalosporins being the class eliciting the highest percentage of resistance; the MDR isolates were all resistant. Among the MDS isolates, all were sensitive to carbapenems and quinolones. The MDR isolates produced less virulence factors such as pyocyanin and lipase, and exhibited lower expression of toxA and lasA genes, whereas the MDS isolates produced less hemolysin and phospholipase C. There was no difference between the groups for alkaline protease production and aprA gene expression. All the isolates produced pyocyanin and expressed lasB and plcH genes. A great genetic diversity was found, and it was possible to observe 28 genetic profiles. Clones were present among the MDR isolates. The occurrence of virulence factors in almost all the isolates studied suggests their high level of pathogenicity, demonstrating that this pathogen is capable of accumulating numerous virulence factors, and in some cases, is associated with multidrug resistance, which makes it difficult to treat these infections.

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Whiteley, Marvin, and E. P. Greenberg. "Promoter Specificity Elements in Pseudomonas aeruginosa Quorum-Sensing-Controlled Genes." Journal of Bacteriology 183, no. 19 (October 1, 2001): 5529–34. http://dx.doi.org/10.1128/jb.183.19.5529-5534.2001.

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ABSTRACT The LasR-dependent and RhlR-dependent quorum-sensing systems are global regulators of gene expression in Pseudomonas aeruginosa. Previous studies have demonstrated that promoter elements of the quorum-sensing-controlled genes lasB andhcnABC are important in density-dependent regulation. We have identified LasR- and RhlR-dependent determinants in promoters of quorum-sensing-controlled genes qsc102, qsc117 (acpP), and qsc131 (phzA to -G) by in silico, deletion, point-mutational, and primer extension analyses. Each of these genes (in addition tolasI and rsaL) is activated by LasR, and qsc117 and qsc131 also respond to RhlR. Point mutations in the promoters of the LasR-specific gene, qsc102, relax specificity so that this promoter can respond to RhlR in addition to LasR. Our findings indicate that quorum-sensing-controlled promoters in P. aeruginosa are either specific for LasR or respond to both LasR and RhlR and that critical bases in the promoter elements determine specificity.

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Kasuya, Tadao, Yasunori Kaneta, and Osamu Sakai. "Pressure Effect on LaSb and CeAs." Journal of the Physical Society of Japan 62, no. 2 (February 15, 1993): 411–15. http://dx.doi.org/10.1143/jpsj.62.411.

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Hasegawa, Akira. "Fermi Surface of LaSb and LaBi." Journal of the Physical Society of Japan 54, no. 2 (February 15, 1985): 677–84. http://dx.doi.org/10.1143/jpsj.54.677.

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Kwon, Y. S., M. Takeshige, T. Suzuki, and T. Kasuya. "Optical properties of CeSb and LaSb." Physica B: Condensed Matter 163, no. 1-3 (April 1990): 328–30. http://dx.doi.org/10.1016/0921-4526(90)90202-6.

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Fallah Tafti, Fazel, Quinn Gibson, Satya Kushwaha, Jason W. Krizan, Neel Haldolaarachchige, and Robert Joseph Cava. "Temperature−field phase diagram of extreme magnetoresistance." Proceedings of the National Academy of Sciences 113, no. 25 (June 7, 2016): E3475—E3481. http://dx.doi.org/10.1073/pnas.1607319113.

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The recent discovery of extreme magnetoresistance (XMR) in LaSb introduced lanthanum monopnictides as a new platform to study this effect in the absence of broken inversion symmetry or protected linear band crossing. In this work, we report XMR in LaBi. Through a comparative study of magnetotransport effects in LaBi and LaSb, we construct a temperature−field phase diagram with triangular shape that illustrates how a magnetic field tunes the electronic behavior in these materials. We show that the triangular phase diagram can be generalized to other topological semimetals with different crystal structures and different chemical compositions. By comparing our experimental results to band structure calculations, we suggest that XMR in LaBi and LaSb originates from a combination of compensated electron−hole pockets and a particular orbital texture on the electron pocket. Such orbital texture is likely to be a generic feature of various topological semimetals, giving rise to their small residual resistivity at zero field and subject to strong scattering induced by a magnetic field.

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Antunes, Marcelo B., John J. Chi, Zhi Liu, Natalia Goldstein-Daruech, James N. Palmer, Jun Zhu, and Noam A. Cohen. "Molecular Basis of Tobacco-Induced Bacterial Biofilms." Otolaryngology–Head and Neck Surgery 147, no. 5 (May 17, 2012): 876–84. http://dx.doi.org/10.1177/0194599812447263.

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Objective To evaluate changes in the expression of biofilm-related genes when exposed to tobacco smoke and oxidative stress. Study Design Experimental, in vitro. Setting Laboratories of Rhinology and Microbiology, University of Pennsylvania. Subjects and Methods Bacterial biofilm mass was measured using crystal violet staining and measurement of the optical density. Biofilm-related genes of the Pseudomonas aeruginosa PAO1 strain ( pilF, flgK, lasI, lasB, rhlA, and algC) were studied following repetitive exposure to exogenous tobacco smoke and hydrogen peroxide. This was done using a reporter plasmid. Results After 1 exposure to smoke, there was no change in biofilm formation. However, after 2 and 3 exposures, the biofilm formed had an increased mass ( P < .05). With respect to oxidative stress in the form of H2O2, bacterial cultures demonstrated a dose- and time-dependent induction of biofilm formation compared with control conditions. Gene expression following repetitive smoke exposure demonstrated an increase in expression of pilF, flgK, algC, and lasI genes ( P < .05); a decrease in rhlA ( P < .05); and no significant change in the lasB gene ( P = 0.1). Gene expression following H2O2 exposure demonstrated an increase in pilF ( P < .05), whereas the other genes failed to demonstrate a statistical change. Conclusions Repetitive tobacco smoke exposure leads to molecular changes in biofilm-related genes, and exposure to oxidative stress in the form of H2O2 induces biofilm growth in PAO1. This could represent adaptative changes due to oxidative stress or chemically mediated through any of the several chemicals encountered in tobacco smoke and may explain increased biofilm formation in microbes isolated from smokers.

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Toder, D. S., S. J. Ferrell, J. L. Nezezon, L. Rust, and B. H. Iglewski. "lasA and lasB genes of Pseudomonas aeruginosa: analysis of transcription and gene product activity." Infection and Immunity 62, no. 4 (1994): 1320–27. http://dx.doi.org/10.1128/iai.62.4.1320-1327.1994.

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Yoshida, Makoto, Keiichi Koyama, Takahiro Tomimatsu, Makoto Shirakawa, Akira Ochiai, and Mitsuhiro Motokawa. "The observation of cyclotron resonance in LaSb." Physica B: Condensed Matter 312-313 (March 2002): 684–85. http://dx.doi.org/10.1016/s0921-4526(01)01233-9.

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Tafti, F. F., Q. D. Gibson, S. K. Kushwaha, N. Haldolaarachchige, and R. J. Cava. "Resistivity plateau and extreme magnetoresistance in LaSb." Nature Physics 12, no. 3 (December 14, 2015): 272–77. http://dx.doi.org/10.1038/nphys3581.

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Yoshida, Makoto, Keiichi Koyama, Takahiro Tomimatsu, Makoto Shirakawa, Akira Ochiai, and Mitsuhiro Motokawa. "Determination of Cyclotron Effective Masses on LaSb." Journal of the Physical Society of Japan 71, no. 7 (July 15, 2002): 1752–56. http://dx.doi.org/10.1143/jpsj.71.1752.

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Li, YongTao, JianRong Huang, LanJuan Li, and LinSheng Liu. "Synergistic Activity of Berberine with Azithromycin against Pseudomonas Aeruginosa Isolated from Patients with Cystic Fibrosis of Lung In Vitro and In Vivo." Cellular Physiology and Biochemistry 42, no. 4 (2017): 1657–69. http://dx.doi.org/10.1159/000479411.

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Background/Aims: Pseudomonas aeruginosa (PA) is one of the major opportunistic pathogens which can cause chronic lung infection of cystic fibrosis (CF). The formation of PA biofilm promotes CF development and restricts the antimicrobial efficacies of current antibiotics. Methods: The antimicrobial effects of azithromycin (AZM) and berberine (BER) alone and in combination were evaluated using microdilution method, checkerboard assay, time-kill test, qRT-PCR analysis and absorption method. The treatments of AZM and/or BER were further evaluated in an animal lung infection model via observing survival rate, bacterial burden and histopathology of lung, the levels of pro-/anti-inflammatory cytokines. Results: AZM-BER were demonstrated to be synergistic against ten clinical PA isolates as well as the standard reference PA ATCC27853, in which PA03 was the most susceptible isolate to AZM-BER with FICI of 0.13 and chosen for subsequent experiments. The synergism of AZM-BER was further confirmed against PA03 in time-kill test and scanning electron microscope (SEM) at their concentrations showing synergism. In PA03, we found that AZM-BER could significantly attenuate productions of a series of virulence factors including alginate, LasA protease, LasB protease, pyoverdin, pyocyanin, chitinase as well as extracellular DNA, and remarkably inhibit the levels of quorum sensing (QS) molecules and the expressions of lasI, lasR, rhlI, rhlR at 1/2×MIC, 1×MIC and 2×MIC. In the infection model, the mice survival were increased markedly, the inflammations of infected lungs were improved greatly along with reduced IL-6, IL-8 and ascended IL-10 at 0.8 mg/kg of AZM combined with 3.2 mg/kg of BER. Conclusion: BER might be a promising synergist to enhance the antimicrobial activity of AZM in vitro and in vivo.

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Irum, Sidra, Kanwal Naz, Nimat Ullah, Zeeshan Mustafa, Amjad Ali, Muhammad Arslan, Kashaf Khalid, and Saadia Andleeb. "Antimicrobial Resistance and Genomic Characterization of Six New Sequence Types in Multidrug-Resistant Pseudomonas aeruginosa Clinical Isolates from Pakistan." Antibiotics 10, no. 11 (November 12, 2021): 1386. http://dx.doi.org/10.3390/antibiotics10111386.

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Pseudomonas aeruginosa (P. aeruginosa) is a major bacterial pathogen associated with a variety of infections with high mortality rates. Most of the clinical P. aeruginosa isolates belong to a limited number of genetic subgroups characterized by multiple housekeeping genes’ sequences (usually 5–7) through the Multi-Locus Sequence Typing (MLST) scheme. The emergence and dissemination of novel multidrug-resistant (MDR) sequence types (ST) in P. aeruginosa pose serious clinical concerns. We performed whole-genome sequencing on a cohort (n = 160) of MDR P. aeruginosa isolates collected from a tertiary care hospital lab in Pakistan and found six isolates belonging to six unique MLST allelic profiles. The genomes were submitted to the PubMLST database and new ST numbers (ST3493, ST3494, ST3472, ST3489, ST3491, and ST3492) were assigned to the respective allele combinations. MLST and core-genome-based phylogenetic analysis confirmed the divergence of these isolates and positioned them in separate branches. Analysis of the resistome of the new STs isolates revealed the presence of genes blaOXA-50, blaPAO, blaPDC, blaVIM-2, aph(3′)-IIb, aac(6′)-II, aac(3)-Id, fosA, catB7, dfrB2, crpP, merP and a number of missense and frame-shift mutations in chromosomal genes conferring resistance to various antipseudomonal antibiotics. The exoS, exoT, pvdE, rhlI, rhlR, lasA, lasB, lasI, and lasR genes were the most prevalent virulence-related genes among the new ST isolates. The different genotypic features revealed the adaptation of these new clones to a variety of infections by various mutations in genes affecting antimicrobial resistance, quorum sensing and biofilm formation. Close monitoring of these antibiotic-resistant pathogens and surveillance mechanisms needs to be adopted to reduce their spread to the healthcare facilities of Pakistan. We believe that these strains can be used as reference strains for future comparative analysis of isolates belonging to the same STs.

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Vandeputte, Olivier M., Martin Kiendrebeogo, Sanda Rajaonson, Billo Diallo, Adeline Mol, Mondher El Jaziri, and Marie Baucher. "Identification of Catechin as One of the Flavonoids from Combretum albiflorum Bark Extract That Reduces the Production of Quorum-Sensing-Controlled Virulence Factors in Pseudomonas aeruginosa PAO1." Applied and Environmental Microbiology 76, no. 1 (October 23, 2009): 243–53. http://dx.doi.org/10.1128/aem.01059-09.

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ABSTRACT Quorum-sensing (QS) regulates the production of key virulence factors in Pseudomonas aeruginosa and other important pathogenic bacteria. In this report, extracts of leaves and bark of Combretum albiflorum (Tul.) Jongkind (Combretaceae) were found to quench the production of QS-dependent factors in P. aeruginosa PAO1. Chromatographic fractionation of the crude active extract generated several active fractions containing flavonoids, as shown by their typical spectral features. Purification and structural characterization of one of the active compounds led to the identification of the flavan-3-ol catechin [(2R,3S)-2-(3,4-dihydroxyphenyl)-3,4-dihydro-1(2H)-benzopyran-3,5,7-triol]. The identity of catechin as one of the active molecules was confirmed by comparing the high-pressure liquid chromatography profiles and the mass spectrometry spectra obtained for a catechin standard and for the active C. albiflorum fraction. Moreover, standard catechin had a significant negative effect on pyocyanin and elastase productions and biofilm formation, as well as on the expression of the QS-regulated genes lasB and rhlA and of the key QS regulatory genes lasI, lasR, rhlI, and rhlR. The use of RhlR- and LasR-based biosensors indicated that catechin might interfere with the perception of the QS signal N-butanoyl-l-homoserine lactone by RhlR, thereby leading to a reduction of the production of QS factors. Hence, catechin, along with other flavonoids produced by higher plants, might constitute a first line of defense against pathogenic attacks by affecting QS mechanisms and thereby virulence factor production.

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Oluwabusola, Emmanuel T., Nursheena Parveen Katermeran, Wee Han Poh, Teo Min Ben Goh, Lik Tong Tan, Oluwatofunmilayo Diyaolu, Jioji Tabudravu, Rainer Ebel, Scott A. Rice, and Marcel Jaspars. "Inhibition of the Quorum Sensing System, Elastase Production and Biofilm Formation in Pseudomonas aeruginosa by Psammaplin A and Bisaprasin." Molecules 27, no. 5 (March 6, 2022): 1721. http://dx.doi.org/10.3390/molecules27051721.

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Natural products derived from marine sponges have exhibited bioactivity and, in some cases, serve as potent quorum sensing inhibitory agents that prevent biofilm formation and attenuate virulence factor expression by pathogenic microorganisms. In this study, the inhibitory activity of the psammaplin-type compounds, psammaplin A (1) and bisaprasin (2), isolated from the marine sponge, Aplysinellarhax, are evaluated in quorum sensing inhibitory assays based on the Pseudomonas aeruginosa PAO1 lasB-gfp(ASV) and rhlA-gfp(ASV) biosensor strains. The results indicate that psammaplin A (1) showed moderate inhibition on lasB-gfp expression, but significantly inhibited the QS-gene promoter, rhlA-gfp, with IC50 values at 14.02 μM and 4.99 μM, respectively. In contrast, bisaprasin (2) displayed significant florescence inhibition in both biosensors, PAO1 lasB-gfp and rhlA-gfp, with IC50 values at 3.53 μM and 2.41 μM, respectively. Preliminary analysis suggested the importance of the bromotyrosine and oxime functionalities for QSI activity in these molecules. In addition, psammaplin A and bisaprasin downregulated elastase expression as determined by the standard enzymatic elastase assay, although greater reduction in elastase production was observed with 1 at 50 μM and 100 μM. Furthermore, the study revealed that bisaprasin (2) reduced biofilm formation in P. aeruginosa.

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Farhangi, Alireza, Amir Peymani, and Hossien Ahmadpour-Yazdi. "Design of a gold nanoprobe for the detection of Pseudomonas aeruginosa elastase gene (lasB)." RSC Advances 10, no. 20 (2020): 11590–97. http://dx.doi.org/10.1039/d0ra00848f.

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Vaitheeswaran, G., V. Kanchana, and M. Rajagopalan. "Electronic and structural properties of LaSb and LaBi." Physica B: Condensed Matter 315, no. 1-3 (April 2002): 64–73. http://dx.doi.org/10.1016/s0921-4526(01)01460-0.

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Kumigashira, H., Hyeong-Do Kim, T. Ito, A. Ashihara, T. Takahashi, T. Suzuki, M. Nishimura, O. Sakai, Y. Kaneta, and H. Harima. "High-resolution angle-resolved photoemission study of LaSb." Physical Review B 58, no. 12 (September 15, 1998): 7675–80. http://dx.doi.org/10.1103/physrevb.58.7675.

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Thanh, Tung Truong, Huy Luong Xuan, and Thang Nguyen Quoc. "Correction: Benzo[d]thiazole-2-thiol bearing 2-oxo-2-substituted-phenylethan-1-yl as potent selective lasB quorum sensing inhibitors of Gram-negative bacteria." RSC Advances 11, no. 48 (2021): 30030. http://dx.doi.org/10.1039/d1ra90142g.

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Correction for ‘Benzo[d]thiazole-2-thiol bearing 2-oxo-2-substituted-phenylethan-1-yl as potent selective lasB quorum sensing inhibitors of Gram-negative bacteria’ by Tung Truong Thanh et al., RSC Adv., 2021, 11, 28797–28808, DOI: 10.1039/D1RA03616E.

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Rigane, E., R. Dutoit, S. Matthijs, N. Brandt, S. Flahaut, and K. S. Belghith. "Characterization of Putative Virulence Factors of Pseudomonas aeruginosa Strain RBS Isolated from a Saltern, Tunisia: Effect of Metal Ion Cofactors on the Structure and the Activity of LasB." BioMed Research International 2020 (July 23, 2020): 1–13. http://dx.doi.org/10.1155/2020/6047528.

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Pseudomonas aeruginosa is a ubiquitous Gram-negative bacterium able to survive in diverse environments such as soil, plants, freshwater, and seawater. P. aeruginosa can be an opportunistic pathogen to humans when their immune system is deficient. Its pathogenicity may be linked to the production of virulence factors. We isolated P. aeruginosa strain RBS from the saltern of Sfax in Tunisia. In this study, we characterized the halotolerance, antibiotic susceptibility, and some virulence factors of strain RBS. High NaCl concentrations inhibited growth and motility. However, biofilm formation was enhanced to protect bacteria against salt stress. Among the 18 antibiotics tested, quinolones and tetracycline showed a significant inhibitory effect on growth, motility, and biofilm formation of strain RBS. β-Lactams, however, did not have any inhibitory effect on neither bacterial growth nor motility. In some cases, resistance was due, in part, to biofilm formation. We also showed that RBS produces two proteases, LasB and AprA, which have been shown to be implicated in host infection. LasB was further characterized to study the role of metal ions in enzyme stability. It possesses two distinct metal ion-binding sites coordinating a calcium and a zinc ion. The effect of metal ion chelation was evaluated as well as substitutions of residues involved in metal ion binding. Impairing metal ion binding of LasB led to a loss of activity and a sharp decrease of stability. Our findings suggest that the binding of both metal ions is interdependent as the two metal ions’ binding sites are linked via a hydrogen bond network.

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Adonizio, Allison, Kok-Fai Kong, and Kalai Mathee. "Inhibition of Quorum Sensing-Controlled Virulence Factor Production in Pseudomonas aeruginosa by South Florida Plant Extracts." Antimicrobial Agents and Chemotherapy 52, no. 1 (October 15, 2007): 198–203. http://dx.doi.org/10.1128/aac.00612-07.

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ABSTRACT Quorum sensing (QS) is a key regulator of virulence and biofilm formation in Pseudomonas aeruginosa and other medically relevant bacteria. Aqueous extracts of six plants, Conocarpus erectus, Chamaesyce hypericifolia, Callistemon viminalis, Bucida buceras, Tetrazygia bicolor, and Quercus virginiana, were examined in this study for their effects on P. aeruginosa virulence factors and the QS system. C. erectus, B. buceras, and C. viminalis caused a significant inhibition of LasA protease, LasB elastase, pyoverdin production, and biofilm formation. Additionally, each plant presented a distinct effect profile on the las and rhl QS genes and their respective signaling molecules, suggesting that different mechanisms are responsible for efficacy. Extracts of all plants caused the inhibition of QS genes and QS-controlled factors, with marginal effects on bacterial growth, suggesting that the quorum-quenching mechanisms are unrelated to static or cidal effects.

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Journal articles on the topic 'Lasb'

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