TLRs play a key role in innate immunity. The biological activity of substituted guanidines was known in the mid-1930s when a series of guanidines and metformin compounds were found to possess bactericidal and disinfectant properties. Int. Cell Fact. Immunology. Goswami et al. Burrows, L. L. Pseudomonas aeruginosa twitching motility: type IV pili in action. 196, 27752788 (2014). GacS/GacA TCS is regulated by sensor kinases RetS (positive regulation) and LadS (negative regulation). Vesicle-mediated export and assembly of pore-forming oligomers of the enterobacterial ClyA cytotoxin. 36, 18691887 (2017). J. Bacteriol. EstA has esterase activity and is involved in rhamnolipid production and biofilm formation.143. J. Immunol. Traditionally, proteases are considered virulence factors, including those that produce cytopathic effects in the host or that have been implicated in manipulating the immune . Forti, F. et al. Chem. Taken together, these observations underscore the critical contribution of the yeast-to-hyphae switch in C. albicans virulence and reinforce the importance of cell-intrinsic and tissue-specific environmental factors in the determination of the C. albicans morphotype under various niches and conditions. BNT162b2 and mRNA-1273 COVID-19 vaccine effectiveness against the SARS-CoV-2 Delta variant in Qatar. Kawai, T. & Akira, S. Signaling to NF-kappaB by Toll-like receptors. Front. Int. Martinon, F., Burns, K. & Tschopp, J. If your research funder has signed Plan S, your open access charges may be covered by your funder through December 31, 2024. Google Scholar. 475, 343347 (2011). & Demuth, D. R. Outer membrane-like vesicles secreted by Actinobacillus actinomycetemcomitans are enriched in leukotoxin. Immunol. Marko, V. A., Kilmury, S. L. N., MacNeil, L. T. & Burrows, L. L. Pseudomonas aeruginosa type IV minor pilins and PilY1 regulate virulence by modulating FimS-AlgR activity. Valentini, M. & Filloux, A. Biofilms and Cyclic di-GMP (c-di-GMP) signaling: lessons from Pseudomonas aeruginosa and other bacteria. made a cocktail with six phages: E215, E217, PAK_P1, PYO2, DEV, and PAK_P4 and showed some effects against clinical P. aeruginosa strains.349 A number of studies showed that phage cocktails possess enhanced efficiency in killing P. aeruginosa compared to single phage therapy.350,351 As strains from patients are distinct, personalized phages combined with antibiotics have also been applied for effective and safe therapy in clinics. J. Biol. 183, 43304344 (2001). Modulation of type III secretion system in Pseudomonas aeruginosa: involvement of the PA4857 gene product. 105, 25622567 (2008). Microorganisms. Multiple sensors control reciprocal expression of Pseudomonas aeruginosa regulatory RNA and virulence genes. Kim, J. Y. et al. Am. TCSs play a significant role in controlling either P. aeruginosa virulence or virulence-related behaviors (such as biofilm formation and antibiotic resistance). Rev. 186, 49464958 (2011). 6, 291 (2021). 15, 649662 (2021). Mol. The substrate protein containing a C-terminal uncleaved secretion signal were recognized by the ABC transporter, were directly transferred across bacterial inner and outer membranes in a one-step process.66 The Has secretion system is composed of HasD (ABC transporter), HasE (adaptor), HasF, and OMF.67 Has secretion system participates in iron regulation by secreting an extracellular haem-binding protein (hasAp).68 Thus far, data relating to T1SS is very limited and its function in pathogenesis and significance for bacterium physiology and fitness are largely unknown, requiring further elucidation in order to know whether it has potential important functions. 8, 24002408 (2006). Cowell, B. Virulence factors are the molecules that assist the bacterium colonize the host at the cellular level. NOD-like receptor protein 3 inflammasome priming and activation in Barretts epithelial cells. Sabnis, A. et al. Crystal structure of Pseudomonas aeruginosa RsaL bound to promoter DNA reaffirms its role as a global regulator involved in quorum-sensing. Bacterial histidine kinases as novel antibacterial drug targets. 7, e1001325 (2011). Sartorio, M. G., Pardue, E. J., Feldman, M. F. & Haurat, M. F. Bacterial outer membrane vesicles: from discovery to applications. 380, 5166 (2008). 2, 155 (2011). Circ. J. Med. e1829 (2016). J. Bacteriol. Breidenstein, E. B., de la Fuente-Nunez, C. & Hancock, R. E. Pseudomonas aeruginosa: all roads lead to resistance. The regulatory repertoire of Pseudomonas aeruginosa AmpC ss-lactamase regulator AmpR includes virulence genes. 2, a012427 (2012). Phytocompound mediated blockage of quorum sensing cascade in ESKAPE pathogens. 8, 333 (2017). Francis, M. S., Wolf-Watz, H. & Forsberg, A. Mol. Using two approaches for encapsulating AMPs, nanotechnology can use an indirect approach where a passive delivery occurs involving a conventional nano-delivery system. Impact Factor 5.882 H Index 74 Impact Factor 4.724 I. Structural and functional characterization of Pseudomonas aeruginosa CupB chaperones. Annu.
Phenotypic and genotypic virulence features of staphylococcal strains 14, e1007074 (2018). 301, 210217 (2009). 78, 63806385 (2012). Ostroff, R. M., Wretlind, B. Some icons or graphic element in the Figures (Figs. Pawluk, A. et al. Nature. TCSs regulatory systems, consisting of sensor kinase and response regulator pairs, play roles in bacterial adaptation by regulating the expression of a variety of extracellular enzymes, virulence factors, and QS molecules. 1, 1029 (2016). Klebsiella surface O polysaccharides (OPS) are protective antigens against infection in animals. Immunol. 67, 198212 (2022). 188, 31693171 (2006). Zhou, C. et al. PLoS Pathog. 592, 256262 (2018). We have summarized TCSs and their roles in controlling the key virulence factors in P. aeruginosa (Table 3). J. Microbiol. The phenazine pyocyanin is a terminal signalling factor in the quorum sensing network of Pseudomonas aeruginosa. 186, 29362945 (2004). Proc. Toxins. Indian J. Microbiol. Phages were applied on the wounds, but the minimal effect was observed.353 With P. aeruginosa being a ubiquitous pathogen that infects lungs and many other organs, further research will investigate how phage therapy would help control chronic CF or COPD diseases. Biophys. Nature. Paeonol attenuates quorum-sensing regulated virulence and biofilm formation in Pseudomonas aeruginosa. Structure of the ExoS GTPase activating domain. Zhao, F. et al. 10, 1218 (2019). Rodrigue, A. et al. McCarthy, K. L. & Paterson, D. L. Increased risk of death with recurrent Pseudomonas aeruginosa bacteremia. Google Scholar. Microbiol. Commun. are commensal bacteria, they can become pathogenic, leading to various types of infections. 17, 820828 (2015). Mikkelsen, H., Ball, G., Giraud, C. & Filloux, A. From a . 10, 1163 (2019). Sutterwala, F. S. et al. 17) are adapted from BioRender.com (2022). 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. Adv. J. Immunol. Overexpression of CupB5 activates alginate overproduction in Pseudomonas aeruginosa by a novel AlgW-dependent mechanism. Mice immunized with DNA encoding a modified Pseudomonas aeruginosa exotoxin A develop protective immunity against exotoxin intoxication.
Microbes and Infection | Journal | ScienceDirect.com by Elsevier Redox Signal. Nivaskumar, M. & Francetic, O. Micro. Volume 14, 2023 Vol 13, 2022 Vol 12, 2021 Vol 11, 2019-2020 Vol 10, 2019 Vol 9, 2018 Vol 8, 2017 Vol 7, 2016 Vol 6, 2015 Vol 5, 2014 Vol 4, 2013 Vol 3, 2012 Vol 2, 2011 Vol 1, 2010. Macromol. e1215 (2017). Fimbriae (pili): molecular basis of Pseudomonas aeruginosa adherence. 305, 276282 (2015). 10, 1701 (2019). Today. Am. CAS As the first line of host defense systems, the innate immune system plays a vital role in battling with P. aeruginosa via multiple mechanisms, such as phagocytosis and inflammatory responses. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. 16, 155 (2016). 205, 22312242 (2020). PLoS One. Berni, B. et al. Nature. Microbiol. 23, e13339 (2021). Mechanisms of antimicrobial resistance in P. aeruginosa. Vasquez-Rifo, A. et al. Li, R. et al. A type VI secretion system trans-kingdom effector is required for the delivery of a novel antibacterial toxin in Pseudomonas aeruginosa. Gupta, R. K., Chhibber, S. & Harjai, K. Acyl homoserine lactones from culture supernatants of Pseudomonas aeruginosa accelerate host immunomodulation. Cadoret, F., Ball, G., Douzi, B. Article About the journal Aims & Scope Microbial Pathogenesis publishes original contributions and reviews about the molecular and cellular mechanisms of infectious diseases. 7, e16436 (2014). 40, 480493 (2016). 19, 11061112 (2000). Microbiol. 1843, 16641673 (2014). However, it is not clear whether CRISPR-Cas systems can regulate antibiotic resistance in P. aeruginosa, which may be studied in future (Fig.
Yehl, K. et al. OMVs may be fused with the host plasma membrane through receptor-mediated endocytosis. Rosenau, F. et al. Retrieved 2014-12-18. Chem. Invest. Both Gram-negative and -positive bacteria detect the local population density by sensing chemical signals and coordinate gene expression and group-beneficial behaviors.156,157 Bacteria produce autoinducer or quoromone as diffusion signaling molecules and release into the environment for communication. Mol. Lin, P. et al. 130, 826831 (1977). Miller, C. L. et al. USA. Two canonical N-acyl L-homoserine lactone (AHL) based (Las and Rhl) and two 2-alkyl-4 quinolones (AQ) based (Pqs and its precursor Hhq) signaling systems.70 These systems connect and coregulate each other. Ma, S., Wozniak, D. J. 285, 89858994 (2010). Submit Manuscript 2 Year 3 Year 4 Year 5 Year Real-Time Prediction Quartile Ranking Acids Res. Yang, N. et al. Surveill. 370, 111 (2015). A. et al. de Regt, A. K. et al. Pseudomonas aeruginosa LasA protease in treatment of experimental staphylococcal keratitis. USA. Garai, P. et al. Infect. CRISPR-Cas13 inhibitors block RNA editing in bacteria and mammalian cells. Engineered bacteriophages for treatment of a patient with a disseminated drug-resistant Mycobacterium abscessus. Biol. Optom. LPS induces respiratory tract infections by regulating epithelial-mesenchymal transition (EMT)-mediated airway remodeling.37 The mutations of LPS can result in attenuated virulence.38,39 Caffeine alleviates the excessive inflammatory response caused by P. aeruginosa infection by inhibiting the activation of LPS-mediated TLR4/MyD88/NF-B/miR-301b signaling pathway, and improves lung tissue injury.40 Notably, LPS mutations confer bacteria gain tolerance to phage infection.41 Taken together, in addition to the direct interaction with the host PRRs receptors, LPS may use its unique molecular features to adjust bacterial pathogenesis and damage host immune defense, ultimately benefiting the fitness and invasive strength. Environ. Rev. Transient receptor potential channel 1 deficiency impairs host defense and proinflammatory responses to bacterial infection by regulating protein kinase calpha signaling. Maura, D. et al. Mutations affecting Leptospira interrogans lipopolysaccharide attenuate virulence. Adv. 278, 3279432800 (2003). Infect. 7, 707 (2019). Grande, K. K., Gustin, J. K., Kessler, E. & Ohman, D. E. Identification of critical residues in the propeptide of LasA protease of Pseudomonas aeruginosa involved in the formation of a stable mature protease. Immunol. Finally, OMVs are being tested in clinical settings either vaccines or therapeutic carriers.58 Taken together, despite the strong interest in research and urgent need in public health, vaccines against P. aeruginosa are still unavailable for clinical application. Biotechnol. Cell. 102, 309314 (2005). Acta. Bacterial-derived OMVs have been characterized as a novel secretion mechanism that can deliver a variety of bacterial proteins and lipids into host cells without direct contact with host cells.42,43,44 OMVs can package and enrich a wide variety of proteins and nucleic acids, including lipoproteins, periplasmic proteins (E. coli cytolysin A, enterotoxigenic E. coli heat-labile enterotoxin, and Actinobacillus actinomycetemcomitans leukotoxin), plasmid containing chromosomal DNA fragments, phage DNA, virulence factors (LPS, alkaline phosphatase, phospholipase C, -lactamase, and Cif et al.45,46 P. aeruginosa secretion of OMVs have been implicated in many virulence-associated behaviors, including the acquisition of drug resistance, the regulation of bacterial density and host immune escape.47,48,49,50,51 Mechanistically, P. aeruginosa secretes OMVs to deliver virulence factors and sRNAs into lung epithelial cells through the diffusion the mucus layer.44,47,52,53,54,55 Some studies also illustrate that OMVs could lead to an increased hydrophobicity of cell surface, resulting in enhanced ability to form biofilms.56 OMVs is controlled by quorum-sensing systems, which enable bacteria to colonize and immune escape.54,57 Interestingly, OMVs are naturally immunogenic and self-adjuvation, making them have potential to be developed as antibacterial vaccine, such as OMV vaccine for Neisseria meningitidis.58,59,60 Therefore, OMVs are not only an important functional constitute, but also a potential biotechnological engineering carrier for vaccination or drug delivery. Dis. Hauser, A. R. The type III secretion system of Pseudomonas aeruginosa: infection by injection. PubMed Central Opin. Crit. T6SS systems have been detected in ~200 Gram-negative bacteria, including P. aeruginosa.109 To compete for survival in the living environment, H1-T6SS kills other bacteria by injecting Tse2 effector molecules into other target bacteria possessing antibacterial activity and providing advantages for P. aeruginosa growth. Chem.
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