B Biol. 43, S49S56 (2006). Antimicrob. Agents Chemother. 364, 122 (2017). To date, many nanoparticles-mediated compounds are in clinical development and several of them have been approved for human therapy, especially cancer therapy, hepatic fibrosis, virus infection, fungal infections, hypercholesterolemia, and pneumonia.344,345,346 In particular, the recently approved lipid nanoparticle (LNP) mRNA vaccines for COVID-19 was an acclaimed success in nanoparticle research for contribution to novel vaccines to combat diseases.347. 43, 1084810860 (2015). 284, 33923403 (2017). Biotechnol. Immunol. Enter journal title, issn or abbr in this box to search . Vaccine formulations can be efficiently targeted by antigen-presenting cells to generate both humoral and cellular immune responses. 194, 57285738 (2012). Development of potent inhibitors of pyocyanin production in Pseudomonas aeruginosa. A novel bacteriophage cocktail reduces and disperses Pseudomonas aeruginosa biofilms under static and flow conditions. & Liang, Z. X. J. Microbiol. Inactivation of CRISPR-Cas systems by anti-CRISPR proteins in diverse bacterial species. 12, 300308 (2014). Rev. Sci. Immun. Google Scholar. M.W. The inflammasome is a multiprotein complex, which is attributed to the production and release of inflammatory cytokines, IL-1 and IL-18.286,287 Recent work reveals that inflammasome is involved in pyroptosis dependent on the cleavage of Gasdermin D, which contributed to the formation of plasma membrane pores, and in turn promoting the release of inflammatory cytokines and pyroptosis.288,289 Typically, inflammasome consists of cytosolic PRRs, ASC (an apoptosis-associated speck-like protein containing a CARD), and caspase 1. J. Mol. Paterson, D. L. & Bonomo, R. A. Extended-spectrum beta-lactamases: a clinical update. Diversity of small RNAs expressed in Pseudomonas species. Martinon, F., Burns, K. & Tschopp, J. * Required, Email(will not be published) Infect. In addition, novel antimicrobial peptides are promising to become the next generation of antimicrobials. J. Med. Microbiol. Preprint at bioRxiv https://doi.org/10.1101/2022.02.23.481616 (2022). 36, 184204 (2007). PubMed P. aeruginosa that was isolated from European populations with a combined resistance was 12.9%.9 Hospital-acquired infection caused by P. aeruginosa continues to produce resistance to conventionally effective antibiotics becoming a main healthcare problem.10 The 2016 EPINE survey found that Escherichia coli and P. aeruginosa are the most common cause of hospital-acquired infections in Spain, P. aeruginosa accounting for 10.5% of clinically isolated bacteria infections.11 The 20112012 HCAIs report that P. aeruginosa caused almost nosocomial 9% of infections, which is the fourth commonest pathogen of the European hospitals.12 Similarly, 7.1% of HCAI are caused by P. aeruginosa in the United States.13 In addition, the 2016 European Center for Disease Prevention and Control (ECDC) epidemiological reported that P. aeruginosa causes a variety of ICU-hospital-acquired infections, including pneumonia flares, urinary tract infections, and bloodstream infections.9,10,14,15 Furthermore, data from China Antimicrobial Surveillance Network (CHINET) (http://www.chinets.com/) identified 301,917 clinically isolated pathogenic strains and found P. aeruginosa was the fourth nosocomial infections after Escherichia coli, Klebsiella pneumoniae, and Staphylococcus aureus, accounting for 7.96%. J. Glob. Microbiol. The impact score (IS), also denoted as Journal impact score (JIS), of an academic journal is a measure of the yearly average number of citations to recent articles published in that journal. In the meantime, to ensure continued support, we are displaying the site without styles Nat. 19, 419426 (2011). Berrazeg, M. et al. Daddaoua, A. et al. Curr. Sci. Schema of P. aeruginosa pathogenesis. Hardy, K. S. et al. & Haagsman, H. P. Outer membrane vesicle induction and isolation for vaccine development. 22, 128 (2021). J. Bacteriol. Physiol. Biotechnol. Pattern recognition receptors and the host cell death molecular machinery. Interaction regulation and inter-conversion of T6SS and T3SS may be especially helpful for coping with complex environmental pressures.110 The switch between T6SS and T3SS is directly regulated by the RNA-binding protein RtcB controlling colonization, establishment, and pathogenicity in P. aeruginosa.111 YbeY regulates T3SS and T6SS secretion systems and biofilm formation by controlling RetS.112 The function of T3SS is regulated by various regulators, including four main regulators genes (exsA, exsC, exsD, and exsE), which is involved in the transcription activation of the aforementioned classical effectors (exoS, exoT, exoU, and exoY).72,113 ExoS is a 48.3kDa protein containing 453 amino acid length. Provvedi R, Sali M, Manganelli R. Mycobacterium tuberculosis virulence: insights and impact on vaccine development. Journal of Pathogens | Hindawi Antibiotics. Plazomicin is a novel semi-synthetic parenteral aminoglycoside that inhibits bacterial protein synthesis, and is shown to inhibit P. aeruginosa growth.337 Plazomicin is assessed in two Phase III randomized controlled trials, with an EPIC trial compared with meropenem in Complicated Urinary Tract Infection (cUTI). Turner, K. H. et al. Microbiol. 56, 1527915283 (2017). Li, M. et al. Front. Virulence - Impact Factor, Overall Ranking, Rating, h Immunol. Adv. 13, 518 (2007). All types of documents are considered, including citable and non citable documents. Kulp, A. MicroRNA-302b augments host defense to bacteria by regulating inflammatory responses via feedback to TLR/IRAK4 circuits. Microbiol. 11, 5559 (2019). FEMS Microbiol. 1961, 111126 (2019). Ghosh, S. et al. Shi, J. et al. These authors contributed equally: Shugang Qin, Wen Xiao, Chuanmin Zhou. 9, 22912299 (2014). Another caveat is that most experiments have not been performed at holistic and/or spatiotemporal levels to evaluate the dynamics, rather a single cell type, specific location, and one or two timepoints. Z., Nikaido, H. & Poole, K. Role of mexA-mexB-oprM in antibiotic efflux in Pseudomonas aeruginosa. Ed. J. Biol. Mol. 17, 112 (2017). Sci. Li, X. et al. Thank you for visiting nature.com. Mol. Baumann, U., Wu, S., Flaherty, K. M. & McKay, D. B. Three-dimensional structure of the alkaline protease of Pseudomonas aeruginosa: a two-domain protein with a calcium binding parallel beta roll motif. J. Bacteriol. Arlehamn, C. S. & Evans, T. J. Pseudomonas aeruginosa pilin activates the inflammasome. Chen, K. et al. J. Med. The recruitment of neutrophils is a sign of inflammatory response activation. Basic Journal Info Country United States Journal ISSN: 21505594, 21505608 Publisher: Landes Bioscience History: 2010-ongoing Journal Hompage: Link How to Get Published: Find out more Research Categories Immunology and Microbiology Medicine Virulence Impact Factor by Web of Science Index The Impact Factor (IF) for the year 2021 is 5.818. Microbiol. Gastroenterol. The pathogenesis of severe malarial disease is not yet fully understood. Microbiol. Biophys. Biochem. Lee, J. Microbiol. Front. Furthermore, our studies reveal an Azu-interacting partner OprC, which is a Cu2+-specific TonB-dependent outer membrane transporter and is also modulated by CueR. The outer membrane of P. aeruginosa is chiefly composed of bilayer phospholipid molecules, LPS and porins embedded in phospholipids. PLoS One. PLoS One. Huang, T. et al. The standard reference for pathogenic and nonpathogenic amoebae is the human parasite <i>Entamoeba histolytica</i>; a direct correlation between virulence and protease expression has been demonstrated for this amoeba. 13, 509519 (2013). Dev. Cell. Progeny phages release and migrate towards infection sites through targeting specific bacteria. J. Bacteriol. Int. Transient receptor potential channel 1 deficiency impairs host defense and proinflammatory responses to bacterial infection by regulating protein kinase calpha signaling. 10, 599606 (2004). Kesty, N. C. & Kuehn, M. J. Incorporation of heterologous outer membrane and periplasmic proteins into Escherichia coli outer membrane vesicles. Immune recognition of Pseudomonas aeruginosa mediated by the IPAF/NLRC4 inflammasome. Front. ^ a b "Master Journal List". 13, 162169 (2012). Specific lipopolysaccharide found in cystic fibrosis airway Pseudomonas aeruginosa. A type I-F anti-CRISPR protein inhibits the CRISPR-Cas surveillance complex by ADP-ribosylation. Hoggarth, A. et al. Mol. Pseudomonas aeruginosa-dependent upregulation of TLR2 influences host responses to a secondary Staphylococcus aureus infection. Quorum sensing controls the Pseudomonas aeruginosa CRISPR-Cas adaptive immune system. EMBO J. KEYWORDS: Peptidase protease A type VI secretion system trans-kingdom effector is required for the delivery of a novel antibacterial toxin in Pseudomonas aeruginosa. 70, 21982205 (2002). Cell. J. Bacteriol. 7, 707 (2019). Microbiol. e110 (2017). Proc. Natl Acad. B. et al. Drug Resist. 80, 951965 (2011). A full-scale network of regulatory understanding of P. aeruginosa virulence is expected to be unveiled, thus, we will be in a much better position for rationale drug design to control Pseudomonas aeruginosa infections. Heussler, G. E. et al. 10, 2931 (2019). 25, 5689 (2020). Many virulence factors are impacted by the alternative sigma factor SigB, the Sar family of DNA-binding proteins (of which SarA is shown), the Agr quorum-sensing system, and further regulators such as SaeRS. While OMVs are detrimental to the host by delivering antibiotic resistance molecules or enzymes (-lactamase), they have been harnessed as alternative delivery vehicles for transporting treatments or vaccines for various diseases including infection and cancer.47,238. Zhang, F., Wen, Y. Clin. Rev. Norepinephrine represses the expression of toxA and the siderophore genes in Pseudomonas aeruginosa. Novel therapeutics for P. aeruginosa. Rev. J. Biol. 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. . Altogether, P. aeruginosa is not a local, but a global major threat to human health. Karash, S., Nordell, R., Ozer, E. A. SJR is a measure of scientific influence of journals that accounts for both the number of citations received by a journal and the importance or prestige of the journals where such citations come from Resistance and virulence of Pseudomonas aeruginosa clinical strains overproducing the MexCD-OprJ efflux pump. Front. Cells Nanomed. 44, D646D653 (2016). Mol. organized figures and formatted the paper; S.Q., X.S., W.X., C.Z., Q.P., X.D., L.L., H.L., and M.W. Virulence impact factor and citations: scientometric PubMed The authors have no financial conflict of interest. NLRC4 inflammasome is shown capable of recognizing needle and inner rod (PrgJ) T3SS proteins, independently of T3SS exotoxins, or intracellular flagellin utilizing different murine NAIP as adaptors.291,292,293,294 Unexpectively, only one factor, human NAIP (hNAIP), has been found, homologous to murine NAIP5, responsible for sensing P. aeruginosa T3SS inner-rod protein PscI and needle protein PscF.295 Apart from T3SS, the T4SS pilin is also capable of activating inflammasome independent of NLRC4 and ASC.153 P. aeruginosa-induced mitochondrial dysfunction also promotes the assembly and activation of NLRC4 via T3SS.296 Mitochondrial ROS and release of mitochondrial DNA are key to NLRC4 activation under P. aeruginosa infection, which is also dependent on autophagy.296 Removal of damaged mitochondria blocks the activation of NLRC4.296 However, AIM2 appears to be dispensable for recognizing and promoting P. aeruginosa infection-induced inflammation in most cases.297, Although several P. aeruginosa components are implicated in activating inflammasome-related immune defense, little is known about how the bacterium evades immune response after inflammasome activation.298 Recent research broadens our knowledge that P. aeruginosa takes advantage of bacterial QS-dependent secretant, including proteases, pyocyanin, and 3-oxo-C12-HSL, to inhibit the activation of NLRC4 or NLR family, pyrin domain containing 3 (NLRP3) inflammasomes.298 A further study supports that pyocyanin specifically inhibits activation of the NLRP3 inflammasome (but not NLRC4 and AIM2) through induced excessive oxidation,299 contrary to the positive role of oxidation in NLRP3 activation.300 Hence, the potential role of oxidation in P. aeruginosa infection and inflammasome activation requires further study.