百日咳博德特氏菌脂多糖A的氨基葡萄糖修饰赋予其对阳离子抗菌肽的抗性，并增强其对外膜扰动的抗性。
Bordetella pertussis lipid A glucosamine modification confers resistance to cationic antimicrobial peptides and increases resistance to outer membrane perturbation.
作者信息
Shah Nita R, Hancock Robert E W, Fernandez Rachel C
机构信息
Department of Microbiology and Immunology, The University of British Columbia, Vancouver, Canada.
Department of Microbiology and Immunology, The University of British Columbia, Vancouver, Canada
出版信息
Antimicrob Agents Chemother. 2014 Aug;58(8):4931-4. doi: 10.1128/AAC.02590-14. Epub 2014 May 27.
Abstract
Bordetella pertussis, the causative agent of whooping cough, has many strategies for evading the human immune system. Lipopolysaccharide (LPS) is an important Gram-negative bacterial surface structure that activates the immune system via Toll-like receptor 4 and enables susceptibility to cationic antimicrobial peptides (CAMPs). We show modification of the lipid A region of LPS with glucosamine increased resistance to numerous CAMPs, including LL-37. Furthermore, we demonstrate that this glucosamine modification increased resistance to outer membrane perturbation.
摘要
百日咳博德特氏菌是百日咳的病原体，它有多种逃避人类免疫系统的策略。脂多糖（LPS）是一种重要的革兰氏阴性细菌表面结构，它通过Toll样受体4激活免疫系统，并使细菌易受阳离子抗菌肽（CAMP）的作用。我们发现，用氨基葡萄糖对LPS的脂质A区域进行修饰可增强对包括LL-37在内的多种CAMP的抗性。此外，我们证明这种氨基葡萄糖修饰增强了对细菌外膜扰动的抗性。
相似文献
1
Bordetella pertussis lipid A glucosamine modification confers resistance to cationic antimicrobial peptides and increases resistance to outer membrane perturbation.
Antimicrob Agents Chemother. 2014 Aug;58(8):4931-4. doi: 10.1128/AAC.02590-14. Epub 2014 May 27.
2
Bordetella pertussis Lipid A Recognition by Toll-like Receptor 4 and MD-2 Is Dependent on Distinct Charged and Uncharged Interfaces.
J Biol Chem. 2015 May 22;290(21):13440-53. doi: 10.1074/jbc.M115.653881. Epub 2015 Apr 2.
3
Reinforcing Lipid A Acylation on the Cell Surface of Acinetobacter baumannii Promotes Cationic Antimicrobial Peptide Resistance and Desiccation Survival.
mBio. 2015 May 19;6(3):e00478-15. doi: 10.1128/mBio.00478-15.
4
AlmG, responsible for polymyxin resistance in pandemic , is a glycyltransferase distantly related to lipid A late acyltransferases.
J Biol Chem. 2017 Dec 22;292(51):21205-21215. doi: 10.1074/jbc.RA117.000131. Epub 2017 Nov 3.
5
Molecular mechanisms of membrane targeting antibiotics.
Biochim Biophys Acta. 2016 May;1858(5):980-7. doi: 10.1016/j.bbamem.2015.10.018. Epub 2015 Oct 26.
6
Glucosamine found as a substituent of both phosphate groups in Bordetella lipid A backbones: role of a BvgAS-activated ArnT ortholog.
J Bacteriol. 2008 Jun;190(12):4281-90. doi: 10.1128/JB.01875-07. Epub 2008 Apr 18.
7
Surveillance of antimicrobial resistance in contemporary clinical isolates of Bordetella pertussis in Ontario, Canada.
Int J Antimicrob Agents. 2014 Jul;44(1):82-4. doi: 10.1016/j.ijantimicag.2014.04.001. Epub 2014 May 2.
8
D-alanine modification of a protease-susceptible outer membrane component by the Bordetella pertussis dra locus promotes resistance to antimicrobial peptides and polymorphonuclear leukocyte-mediated killing.
J Bacteriol. 2013 Nov;195(22):5102-11. doi: 10.1128/JB.00510-13. Epub 2013 Sep 6.
9
Antimicrobial Susceptibility and Molecular Detection of Pertactin-producing and Pertactin-Deficient Bordetella pertussis.
Pediatr Infect Dis J. 2017 Jan;36(1):119-121. doi: 10.1097/INF.0000000000001366.
10
Enzymatic modification of lipid A by ArnT protects Bordetella bronchiseptica against cationic peptides and is required for transmission.
Infect Immun. 2014 Feb;82(2):491-9. doi: 10.1128/IAI.01260-12. Epub 2013 Oct 14.
引用本文的文献
1
Determining the LPS structural features that influence TLR4 downstream signaling.
Front Microbiol. 2025 Feb 25;16:1540534. doi: 10.3389/fmicb.2025.1540534. eCollection 2025.
2
Polymyxin Resistance and Heteroresistance Are Common in Clinical Isolates of Species and Correlate with Modifications of the Lipid A Moiety of Lipopolysaccharide.
Microbiol Spectr. 2023 Feb 14;11(1):e0372922. doi: 10.1128/spectrum.03729-22. Epub 2022 Dec 15.
3
Bacterial resistance to antibacterial agents: Mechanisms, control strategies, and implications for global health.
Sci Total Environ. 2023 Feb 20;860:160461. doi: 10.1016/j.scitotenv.2022.160461. Epub 2022 Nov 23.
4
Avirulent phenotype promotes adaptation to the intramacrophage environment.
Emerg Microbes Infect. 2023 Dec;12(1):e2146536. doi: 10.1080/22221751.2022.2146536.
5
Harnessing the Role of Bacterial Plasma Membrane Modifications for the Development of Sustainable Membranotropic Phytotherapeutics.
Membranes (Basel). 2022 Sep 22;12(10):914. doi: 10.3390/membranes12100914.
6
Bps polysaccharide of Bordetella pertussis resists antimicrobial peptides by functioning as a dual surface shield and decoy and converts Escherichia coli into a respiratory pathogen.
PLoS Pathog. 2022 Aug 15;18(8):e1010764. doi: 10.1371/journal.ppat.1010764. eCollection 2022 Aug.
7
The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.
PLoS Pathog. 2022 Apr 8;18(4):e1010402. doi: 10.1371/journal.ppat.1010402. eCollection 2022 Apr.
8
Pathogenicity and virulence of and its adaptation to its strictly human host.
Virulence. 2021 Dec;12(1):2608-2632. doi: 10.1080/21505594.2021.1980987.
9
Has resistance to chlorhexidine increased among clinically-relevant bacteria? A systematic review of time course and subpopulation data.
PLoS One. 2021 Aug 19;16(8):e0256336. doi: 10.1371/journal.pone.0256336. eCollection 2021.
10
RNase III and RNase E Influence Posttranscriptional Regulatory Networks Involved in Virulence Factor Production, Metabolism, and Regulatory RNA Processing in Bordetella pertussis.
mSphere. 2021 Aug 25;6(4):e0065021. doi: 10.1128/mSphere.00650-21. Epub 2021 Aug 18.
本文引用的文献
1
Enzymatic modification of lipid A by ArnT protects Bordetella bronchiseptica against cationic peptides and is required for transmission.
Infect Immun. 2014 Feb;82(2):491-9. doi: 10.1128/IAI.01260-12. Epub 2013 Oct 14.
2
D-alanine modification of a protease-susceptible outer membrane component by the Bordetella pertussis dra locus promotes resistance to antimicrobial peptides and polymorphonuclear leukocyte-mediated killing.
J Bacteriol. 2013 Nov;195(22):5102-11. doi: 10.1128/JB.00510-13. Epub 2013 Sep 6.
3
Fortifying the barrier: the impact of lipid A remodelling on bacterial pathogenesis.
Nat Rev Microbiol. 2013 Jul;11(7):467-81. doi: 10.1038/nrmicro3047. Epub 2013 Jun 10.
4
Minor modifications to the phosphate groups and the C3' acyl chain length of lipid A in two Bordetella pertussis strains, BP338 and 18-323, independently affect Toll-like receptor 4 protein activation.
J Biol Chem. 2013 Apr 26;288(17):11751-60. doi: 10.1074/jbc.M112.434365. Epub 2013 Mar 6.
5
The Pseudomonas aeruginosa PhoP-PhoQ two-component regulatory system is induced upon interaction with epithelial cells and controls cytotoxicity and inflammation.
Infect Immun. 2012 Sep;80(9):3122-31. doi: 10.1128/IAI.00382-12. Epub 2012 Jun 18.
6
Pertussis: a matter of immune modulation.
FEMS Microbiol Rev. 2011 May;35(3):441-74. doi: 10.1111/j.1574-6976.2010.00257.x. Epub 2011 Jan 5.
7
Substitution of the Bordetella pertussis lipid A phosphate groups with glucosamine is required for robust NF-kappaB activation and release of proinflammatory cytokines in cells expressing human but not murine Toll-like receptor 4-MD-2-CD14.
Infect Immun. 2010 May;78(5):2060-9. doi: 10.1128/IAI.01346-09. Epub 2010 Feb 22.
8
Glucosamine found as a substituent of both phosphate groups in Bordetella lipid A backbones: role of a BvgAS-activated ArnT ortholog.
J Bacteriol. 2008 Jun;190(12):4281-90. doi: 10.1128/JB.01875-07. Epub 2008 Apr 18.
9
Agar and broth dilution methods to determine the minimal inhibitory concentration (MIC) of antimicrobial substances.
Nat Protoc. 2008;3(2):163-75. doi: 10.1038/nprot.2007.521.
10
Antimicrobial peptides in the airway.
Curr Top Microbiol Immunol. 2006;306:153-82. doi: 10.1007/3-540-29916-5_6.
Zotero 插件