62186, the first from a Gram-negative bacterium. PLoS Pathog. Methods Clin. Infect. The phenazine pyocyanin is a terminal signalling factor in the quorum sensing network of Pseudomonas aeruginosa. Yarlagadda, V. & Wright, G. D. Membrane-active rhamnolipids overcome aminoglycoside resistance. Acta. Front. J. Glob. Song, F., Wang, H., Sauer, K. & Ren, D. Cyclic-di-GMP and oprF are involved in the response of Pseudomonas aeruginosa to substrate material stiffness during attachment on polydimethylsiloxane (PDMS). Outer membrane protein I of Pseudomonas aeruginosa is a target of cationic antimicrobial peptide/protein. PLoS Biol. PubMed J. Am. Annu. Sultan, M., Arya, R. & Kim, K. K. Roles of two-component systems in Pseudomonas aeruginosa virulence. Wang, T. et al. Del Tordello, E., Danilchanka, O., McCluskey, A. J. e112 (2016). Crit. Immunological evaluation of an alginate-based conjugate as a vaccine candidate against Pseudomonas aeruginosa. Rev. Proc. Klein, G. & Raina, S. Small regulatory bacterial RNAs regulating the envelope stress response. Nat. Commun. Research has been conducted with a CRISPR-Cas system that targets endogenous genes to alter host defense.324 To conquer the bacterial immune response for promoting phage replication, phages should gain access to do the job by evolving an anti-CRISPR system (Acrs). An excellent such application was reported by Forti et al., who constructed phage cocktails based on the genomic information and host range.349 Clinical trials of phage therapy have shown viable and sustained efficacy in therapy. Zhou, C. M. et al. EMBO J. A. Structural and molecular mechanism of CdpR involved in quorum-sensing and bacterial virulence in Pseudomonas aeruginosa. Dis. 132, 98579872 (2010). Nucleic Acids Res. Eye Res. 34, 349357 (2009). Pseudomonas aeruginosa magnesium transporter MgtE inhibits type III secretion system gene expression by stimulating rsmYZ transcription. 54, 10901103 (2004). Zhao, F., Wang, Q., Zhang, Y. USA. Microbiol. Chem. 32, 6872 (2019). Soc. Genome editing and nucleic acid-based antibiotics, such as single-stranded DNA (ssDNA), double-stranded DNA (dsDNA), plasmid DNA, and ssRNA358 have emerged as the new types of antimicrobials. Microbiol. J. Biol. Immunol. Cohen, T. S. & Prince, A. S. Activation of inflammasome signaling mediates pathology of acute P. aeruginosa pneumonia. Nature. Agents Chemother. International Collaboration accounts for the articles that have been produced by researchers from several countries. The toxic compounds derived from metabolism or antimicrobials inside bacterial cells are harmful to bacterial survival, and require mechanisms to expel. 7, 654665 (2009). Front. Immunol. van den Berg, B. 29, 377384 (2017). Pseudomonas aeruginosa survives in epithelia by ExoS-mediated inhibition of autophagy and mTOR. 49, 479487 (2005). The outer membrane of P. aeruginosa is chiefly composed of bilayer phospholipid molecules, LPS and porins embedded in phospholipids. Xin, X. F., Kvitko, B. Kilmury, S. L. N. & Burrows, L. L. The Pseudomonas aeruginosa PilSR Two-Component System Regulates Both Twitching and Swimming Motilities. Diggle, S. P. et al. Drug Resist. Pulm. 23, 1009 (2018). Int. J. Bacteriol. Stanton, B. Volume 93, Issue 3 p. 1343-1350. REVIEW. 6, 660 (2015). Infect. Proc. Thank you for visiting nature.com. Structure of exotoxin A of Pseudomonas aeruginosa at 3.0-Angstrom resolution. Sci. Nat. (5) How to better identify new host factors for improved immunity against this bacterium? Microbiol. Eravacycline is a novel fluorocycline that is evaluated for antimicrobial activity against anaerobic Gram-negative and Gram-positive bacteria. Zhao, F. et al. & Ohman, D. E. Identification of the histidine protein kinase KinB in Pseudomonas aeruginosa and its phosphorylation of the alginate regulator algB. Chem. Revisiting quorum sensing: discovery of additional chemical and biological functions for 3-oxo-N-acylhomoserine lactones. Cells. OMVs may be fused with the host plasma membrane through receptor-mediated endocytosis. The regulation of all these virulence factors is cell density-dependent through release of autoinducers of critical quorum sensing (QS) (e.g., Las, Rhl, Pqs, and Iqs), a mass communication system . Wurtele, M. et al. 4 ExPEC have several virulence factors (VFs) that may play a role in infection by enabling the bacterial cells to move into the host and disseminate. J. Lett. 1, 16085 (2016). Lin, P. et al. Cell. J. Biol. Alav, I. et al. Ernst, R. K. et al. Mol. Biswaro, L. S. et al. Bleves, S. et al. The activation of QS genes generally requires a large number of regulatory factors to control receptor expression or function, and/or to coregulate some QS-controlled target genes since the QS systems are functional diverse, organizational complex, and consisting of a spectrum of key regulators (including rpoS, vqsR, mvfR, rhlR, rsaL et al. Yang, D. et al. 16, 20012 (2011). Oligoribonuclease is required for the type III secretion system and pathogenesis of Pseudomonas aeruginosa. Environ. Cathcart, G. R. et al. Positive control of swarming, rhamnolipid synthesis, and lipase production by the posttranscriptional RsmA/RsmZ system in Pseudomonas aeruginosa PAO1. Rev. Biotechnol. Alves, D. R. et al. & Lithgow, T. The TAM: a translocation and assembly module of the beta-barrel assembly machinery in bacterial outer membranes. Folia Microbiol. Pseudomonas aeruginosa regulatory protein AnvM controls pathogenicity in anaerobic environments and impacts host defense. A novel copper-sensing two-component system for inducing Dsb gene expression in bacteria. 55, 26702678 (2011). Evolution of the number of total citation per document and external citation per document (i.e. Read more. J. Bacteriol. 52, 24552462 (2008). The Pseudomonas aeruginosa reference strain PA14 displays increased virulence due to a mutation in ladS. Goswami, M., Espinasse, A. Am. Biotechnol. & Kuehn, M. J. Miller, C. L. et al. The PprA-PprB two-component system activates CupE, the first non-archetypal Pseudomonas aeruginosa chaperone-usher pathway system assembling fimbriae. Cornea. EstA has esterase activity and is involved in rhamnolipid production and biofilm formation.143. Laskowski, M. A., Osborn, E. & Kazmierczak, B. I. Francis, V. I., Stevenson, E. C. & Porter, S. L. Two-component systems required for virulence in Pseudomonas aeruginosa. Paeonol attenuates quorum-sensing regulated virulence and biofilm formation in Pseudomonas aeruginosa. As an active antibiotic against Enterobacteriacease producing CTX-M-15, Zidebactam has some effects against Enterobacteriaceae and P. aeruginosa.339 Although we only reviewed a small portion of ongoing development of new therapeutics for P. aeruginosa with some hope, development of effective therapeutics to counter the growing drug resistance is still challenging. Plazomicin: a novel aminoglycoside for the treatment of resistant Gram-negative bacterial infections. 95, 2226 (2002). Dev. Sin. Virulence- - Find Impact Factor of Journal - ResearchBite Host and pathogen response to bacteriophage engineered against Mycobacterium abscessus lung infection. Environ. 156, 14151423 (2010). 195, 21262135 (2013). Yahr, T. L., Goranson, J. 286, 15611565 (1999). Miller, L. C. et al. The recruitment of neutrophils is a sign of inflammatory response activation. Vaccines based on these components have shown effects against homologous strains, but no effect against different serotypes. Mol. This article broadly reviews the recent progress in P. aeruginosa research towards the regulatory and functional mechanisms of virulence factors, gene expression regulators, secretion systems, quorum sensing, and antibiotic resistance, as well as host-pathogen interaction, new technologic advances, and therapeutic development (Fig. participated in different parts of writing. Ramjeet, M. et al. Environ. Nat. Med. P. aeruginosa with arbapenem-resistance is listed among the critical group of pathogens by WHO, which urgently need novel antibiotics in the clinics.8. The role of CRISPR-Cas systems in virulence of pathogenic bacteria. Bioeng. 586, 31933199 (2012). PubMed Central Chakravarty, S. et al. the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in T6SS can divide into two distinct forms: phage tail-like structure and transmembrane complex, which can be exploited to create multivalent nanoparticle delivery of vaccine antigens. PLoS One. Lee, P. A., Tullman-Ercek, D. & Georgiou, G. The bacterial twin-arginine translocation pathway. 67, 23712376 (1999). 7, e16436 (2014). 8, 287 (2007). 149, 22912299 (2003). T4SS assembly system is evolutionarily associated with T2SS contributing to the process of assembly and disassembly of pili. 43, S49S56 (2006). Miao, E. A. et al. Jepkorir, G. et al. Antimicrobial peptides and nanotechnology, recent advances and challenges. 3, 685695 (2002). Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome. Reduced virulence of a hfq mutant of Pseudomonas aeruginosa O1. Filloux, A., Michel, G. & Bally, M. GSP-dependent protein secretion in gram-negative bacteria: the Xcp system of Pseudomonas aeruginosa. Qin, S. et al. Safari Zanjani, L. et al. USA. 163, 685691 (2012). Pang, Z. et al. Kulp, A. 187, 43274337 (2005). Sebastian-Valverde, M. & Pasinetti, G. M. The NLRP3 inflammasome as a critical actor in the inflammaging process. Biophys. Quorum sensing controls the Pseudomonas aeruginosa CRISPR-Cas adaptive immune system. In contrast, the exoproteins of two-step secretion system are first exported to the periplasm through the Sec or Tat system, and then crossing outer membranes through specific secretion mechanisms. Nature. RsaL provides quorum sensing homeostasis and functions as a global regulator of gene expression in Pseudomonas aeruginosa. Multiple lines of evidence suggest that the chief mechanism for P. aeruginosa success in infection is highly related to its stubborn resistance to antibiotics or other therapeutics, which is regulated by the efflux pump. Sensors. Year: Impact Factor (IF) Total Articles: Total Cites: 2022 (2023 update) 5.2-6972: 2021: 5.428-6725: 2020: . Microbiology. 123, 233241 (2018). Science. 48, 930940 (1995). Microbiol. Natl Acad. Creating a synthetic phage with desired characteristics and genomic content would be a creative approach.355 Recently, mutations in phage host-range-determining regions (HRDRs) to cope with resistance mutation of bacteria have been implemented as an effective method to prevent Escherichia coli infection.41 Engineered bacteriophages BPs33HTH_HRM10 and D29_HRMGD40 cocktail cured a cystic fibrosis patient with a disseminated drug-resistant Mycobacterium abscessus, which shows that the therapeutics of engineered phages to break the evolutionary constraints, holding great potential to create the next-generation of antibacterial antimicrobials.356,357 In spite of recent progress, the strategy for phage therapy is highly difficult. Today. CAS Virulence Journal metrics Journal metrics Usage 850K annual downloads/views Citation metrics 5.428 (2021) Impact Factor Q2 Impact Factor Best Quartile 6.735 (2021) 5 year IF 7.1 (2021) CiteScore (Scopus) Q1 (2021) CiteScore Best Quartile 1.378 (2021) SNIP 1.107 (2021) SJR Speed/acceptance 17 days avg. Marraffini, L. A. CRISPR-Cas immunity in prokaryotes. J. Bacteriol. Acta. Internet Explorer). Mol. 110, 375384 (2020). Kazmierczak, B. I. 65, 329338 (2020). 592, 256262 (2018). https://doi.org/10.1038/s41392-022-01056-1, DOI: https://doi.org/10.1038/s41392-022-01056-1. 9, 113118 (1986). Appl. 189, 799811 (2014). A novel mechanism of inhibition by phenylthiourea on PvdP, a tyrosinase synthesizing pyoverdine of Pseudomonas aeruginosa. 102, 63776384 (2011). Virulence - Impact Factor & Score 2023 A macromolecular approach to eradicate multidrug resistant bacterial infections while mitigating drug resistance onset. J. Bacteriol. from submission to first decision Ramirez, M. S. & Tolmasky, M. E. Aminoglycoside modifying enzymes. Hence, targeting this mechanism such as inhibiting the critical efflux pumpmexAB-oprM or enhancing the repressormexR, will likely reveal new strategies to overcome antibiotic resistance mechanisms in the bacterium and achieve the improved treatment efficacy.244. Dis. Biological functions and biogenesis of secreted bacterial outer membrane vesicles. journal self-citations removed) received by a journal's published documents during the three previous years. J. Bacteriol. 55, 56765684 (2011). Chem. Download citations Download PDFs. Quality-controlled small-scale production of a well-defined bacteriophage cocktail for use in human clinical trials. The structure of the toxin and type six secretion system substrate Tse2 in Complex with its immunity protein. Beier, D. & Gross, R. Regulation of bacterial virulence by two-component systems. Dadashi, M. et al. 7, 707 (2019). & Wu, Y. Leo, J. C., Grin, I. de Regt, A. K. et al. Protein secretion systems in Pseudomonas aeruginosa: a wealth of pathogenic weapons. One-step secretion system exoproteins are directly absorbed into the cytoplasm through their cognate secretion mechanism. Garner, A. L. et al. Goswami et al. Exploiting CRISPR-Cas nucleases to produce sequence-specific antimicrobials. A Pseudomonas aeruginosa TIR effector mediates immune evasion by targeting UBAP1 and TLR adaptors. Hence, a multivalent nanoparticle strategy is considered a superior means and is used in vaccine delivery with P. aeruginosa, specifically to target T6SS. 17) are adapted from BioRender.com (2022). Res. Faure, E. et al. Article Free Access. e110 (2017). Pu, Q. et al. Biophys. Liang, H. et al. 160, 10071019 (2014). Chem. Lau, C. H. & Suh, Y. 362, 240242 (2018). 66, 15571565 (2007). 79, 7587 (2011). 101, 162171 (2018). This review analyzes virulence factors from the viewpoint of the damage-response framework of microbial pathogenesis, which defines virulence factor as microbial components that . 44, 16591666 (2016). Extraintestinal pathogenic E. coli (ExPEC) strains, cause a variety of infections, including urinary tract infections (UTI), sepsis and neonatal meningitis. Interaction of native and N-terminally truncated inhibitor proteins with Pseudomonas metalloproteinases. mBio. 343, 8084 (2014). Rodrigue, A. et al. Mutation of lasA and lasB reduces Pseudomonas aeruginosa invasion of epithelial cells. Lin, Y. M. et al. The MgtC and OprF of PAO1 regulate T3SS and ExoS-induced host macrophage damage.77 The T3SS is positively regulated by PsrA,78 HigB,79 Vfr,80 and DeaD,81 but negatively regulated by MexT,82 AlgZR, GacAS/LadS/RetS,83,84,85,86,87,88 and MgtE.89 No only for P. aeruginosa, the T3SS is a highly important secretion mechanism for Gram-negative bacterial invasion factors, which may also facilitate the bacterial evasion from the host immune responses to establish invasion, colonization, replication, and spread. Rev. Cowell, B. Sci. Annu. The Azu-OprC-mediated Cu2+ transport network may contribute to P. aeruginosa virulence. Schultz, M. J. et al. 5, 166172 (2002). 22, 135 (2021). 14, e1007074 (2018). Science. The drawback of using nanoparticle structures is the likelihood that host immune responses may be activated against the delivery system, which can prohibit the repeated delivery.340 Future experiments need to be conducted to control antigen exposure to generate a uniform particle. Microbiol. 25, 5689 (2020). For some cells that are difficult to transfect, such as primary cells, stem cells, undifferentiated cells, etc., the use of lentiviral vectors has shown versatility to greatly improve the transduction efficiency of the target gene or the target shRNA. Microbiol. & Beyaert, R. Structure and function of the Type III secretion system of Pseudomonas aeruginosa. Sun, J. 12, e1006032 (2016). Lehman, H. K. & Segal, B. H. The role of neutrophils in host defense and disease. Sana, T. G. et al. 53, 21122125 (2014). Chem. Research shows that a large amount of hex-acylated lipid A from LPS is isolated from infected patients, which is a strong TLR4 agonist, capable of activating TLR4-dependent inflammatory response.271,272 In addition, several TLR4 co-receptors MD-2 and CD14 are indicated necessary for TLR4 recognition of LPS and TLR4 activation.273 Airway epithelial cells and macrophages, both expressed TLR4 in the cell membrane, serve as the first line of host defense for the initial contact to P. aeruginosa. Bacteria can acquire antibiotic resistance through mutations or horizontal gene transfer.255,256 Mutations of OprD in P. aeruginosa confers resistance to carbapenems234 and mutations of DNA gyrase (GyrA) causes resistance to quinolone antibiotics.257 Importantly, mutations in the -lactamase gene ampC causes a significant increase in resistance to cephalosporins.258 There are already a host of enzymes in this bacterium may counter antibiotics while it continues to gain new resistance factors, which is debatably the biggest challenge for drug industry and scientific research. 3-Hydroxy-1-alkyl-2-methylpyridine-4(1H)-thiones: inhibition of the Pseudomonas aeruginosa virulence factor LasB. J. Leukoc. Optom. Microbiol. & Hancock, R. E. Role of Pseudomonas aeruginosa outer membrane protein OprH in polymyxin and gentamicin resistance: isolation of an OprH-deficient mutant by gene replacement techniques. 102, 309314 (2005). 19, 419426 (2011). Front. 10, 417426 (2002). Genomic and metabolic characteristics of the pathogenicity in Pseudomonas aeruginosa. Hayashi, F. et al.
