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Staphylococcus aureus is a leading cause of bacterial pneumonia, and we have shown previously that type I interferon (IFN) contributes to the pathogenesis of this disease. In this study, we screened 75 S. aureus strains for their ability to induce type I and III IFN. Both cytokine pathways were differentially stimulated by various S. aureus strains independently of their isolation sites or methicillin resistance profiles. These induction patterns persisted over time, and type I and III IFN generation differentially correlated with tumor necrosis factor alpha production. Investigation of one isolate, strain 126, showed a significant defect in type I IFN induction that persisted over several time points. The lack of induction was not due to differential phagocytosis, subcellular location, or changes in endosomal acidification. A correlation between reduced type I IFN induction levels and decreased autolysis and lysostaphin sensitivity was found between strains. Strain 126 had a decreased rate of autolysis and increased resistance to lysostaphin degradation and host cell-mediated killing. This strain displayed decreased virulence in a murine model of acute pneumonia compared to USA300 (current epidemic strain and commonly used in research) and had reduced capacity to induce multiple cytokines. We observed this isolate to be a vancomycin-intermediate S. aureus (VISA) strain, and reduced Ifnb was observed with a defined mutation in walK that induces a VISA phenotype. Overall, this study demonstrates the heterogeneity of IFN induction by S. aureus and uncovered an interesting property of a VISA strain in its inability to induce type I IFN production.

Titel:	Differential Induction of Type I and III Interferons by Staphylococcus aureus .
Autor/in / Beteiligte Person:	Peignier, A ; Planet, PJ ; Parker, D
Link:	Full Text Finder (Volltext)
Zeitschrift:	Infection and immunity, Jg. 88 (2020-09-18), Heft 10
Veröffentlichung:	Washington, DC : American Society For Microbiology ; <i>Original Publication</i>: [Bethesda, Md.] American Society for Microbiology., 2020
Medientyp:	academicJournal
ISSN:	1098-5522 (electronic)
DOI:	10.1128/IAI.00352-20
Schlagwort:	Animals Anti-Bacterial Agents pharmacology Bacterial Load Bacterial Proteins genetics Cells, Cultured Drug Resistance, Bacterial genetics Lysostaphin pharmacology Mice Microbial Sensitivity Tests Mutation Pneumonia, Staphylococcal immunology Pneumonia, Staphylococcal microbiology Signal Transduction Staphylococcal Infections microbiology Staphylococcus aureus drug effects Staphylococcus aureus isolation & purification Vancomycin pharmacology Virulence Cytokines immunology Interferon Type I immunology Staphylococcal Infections immunology Staphylococcus aureus pathogenicity
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural Language: English [Infect Immun] 2020 Sep 18; Vol. 88 (10). <i>Date of Electronic Publication: </i>2020 Sep 18 (<i>Print Publication: </i>2020). MeSH Terms: Cytokines / immunology ; Interferon Type I / immunology ; Staphylococcal Infections / immunology ; Staphylococcus aureus / pathogenicity ; Animals ; Anti-Bacterial Agents / pharmacology ; Bacterial Load ; Bacterial Proteins / genetics ; Cells, Cultured ; Drug Resistance, Bacterial / genetics ; Lysostaphin / pharmacology ; Mice ; Microbial Sensitivity Tests ; Mutation ; Pneumonia, Staphylococcal / immunology ; Pneumonia, Staphylococcal / microbiology ; Signal Transduction ; Staphylococcal Infections / microbiology ; Staphylococcus aureus / drug effects ; Staphylococcus aureus / isolation & purification ; Vancomycin / pharmacology ; Virulence References: Hepatology. 2014 Apr;59(4):1262-72. (PMID: 23929627) ; Sci Signal. 2017 Jul 18;10(488):. (PMID: 28720717) ; PLoS Pathog. 2014 Feb 20;10(2):e1003951. (PMID: 24586160) ; Lancet. 2002 May 25;359(9320):1819-27. (PMID: 12044378) ; Clin Microbiol Infect. 2017 Oct;23(10):767-773. (PMID: 28396035) ; Nat Genet. 2013 Feb;45(2):164-71. (PMID: 23291588) ; Int J Mol Sci. 2019 Mar 21;20(6):. (PMID: 30901970) ; Cytokine Growth Factor Rev. 2004 Feb;15(1):33-48. (PMID: 14746812) ; Lancet. 2006 Mar 4;367(9512):731-9. (PMID: 16517273) ; J Gen Microbiol. 1952 Feb;6(1-2):95-107. (PMID: 14927856) ; Clin Microbiol Rev. 1997 Jul;10(3):505-20. (PMID: 9227864) ; Cell Microbiol. 2012 Oct;14(10):1513-21. (PMID: 22747834) ; Clin Microbiol Rev. 2013 Apr;26(2):185-230. (PMID: 23554414) ; Clin Infect Dis. 2017 Nov 13;65(11):1921-1923. (PMID: 29020322) ; Front Immunol. 2017 Mar 22;8:313. (PMID: 28382038) ; J Antimicrob Chemother. 2012 Sep;67(9):2069-89. (PMID: 22618862) ; PLoS One. 2012;7(1):e29573. (PMID: 22253738) ; Med Microbiol Immunol. 2015 Apr;204(2):215-26. (PMID: 25187407) ; J Biol Chem. 2013 Oct 11;288(41):29440-52. (PMID: 23970550) ; Cytokine. 2015 Dec;76(2):480-495. (PMID: 26228976) ; Nat Immunol. 2015 Aug;16(8):802-9. (PMID: 26194286) ; J Bacteriol. 2003 Dec;185(24):7103-10. (PMID: 14645269) ; Cold Spring Harb Perspect Biol. 2014 Oct 09;7(1):a016246. (PMID: 25301932) ; Nat Rev Dis Primers. 2018 May 31;4:18033. (PMID: 29849094) ; Yale J Biol Med. 2017 Jun 23;90(2):269-281. (PMID: 28656013) ; Gastroenterology. 2006 Dec;131(6):1887-98. (PMID: 17087946) ; J Immunol. 2008 Feb 15;180(4):2474-85. (PMID: 18250457) ; mBio. 2013 Feb 12;4(1):e00537-12. (PMID: 23404398) ; Front Microbiol. 2016 Oct 13;7:1601. (PMID: 27790199) ; Infect Genet Evol. 2014 Jan;21:575-82. (PMID: 23567819) ; N Engl J Med. 2005 Apr 7;352(14):1445-53. (PMID: 15814880) ; Mol Microbiol. 2007 Jul;65(1):180-200. (PMID: 17581128) ; Front Cell Infect Microbiol. 2012 Apr 24;2:43. (PMID: 22919634) ; J Immunol. 2012 Oct 15;189(8):4040-6. (PMID: 22962685) ; J Bacteriol. 2007 Nov;189(21):7573-80. (PMID: 17827298) ; J Infect Dis. 1998 Jul;178(1):164-71. (PMID: 9652436) ; J Immunol. 2011 Apr 15;186(8):4541-5. (PMID: 21398614) ; Cell Microbiol. 2014 Apr;16(4):451-65. (PMID: 24164701) ; Nat Rev Microbiol. 2009 Sep;7(9):629-41. (PMID: 19680247) ; Front Microbiol. 2018 Nov 16;9:2725. (PMID: 30524387) ; J Bacteriol. 1999 Jun;181(12):3666-73. (PMID: 10368139) ; Immunol Rev. 2013 Sep;255(1):25-39. (PMID: 23947345) ; Immunity. 2019 Apr 16;50(4):907-923. (PMID: 30995506) ; J Glob Antimicrob Resist. 2014 Dec;2(4):213-224. (PMID: 27873679) ; Appl Microbiol Biotechnol. 2008 Sep;80(4):555-61. (PMID: 18607587) ; Nat Commun. 2019 Jul 11;10(1):3067. (PMID: 31296851) ; Antimicrob Agents Chemother. 2000 Oct;44(10):2845-7. (PMID: 10991869) ; Eur J Immunol. 2018 Oct;48(10):1707-1716. (PMID: 30051912) ; Nat Immunol. 2003 Jan;4(1):69-77. (PMID: 12483210) ; J Antimicrob Chemother. 1989 Nov;24(5):637-45. (PMID: 2599989) ; PLoS Pathog. 2013;9(10):e1003682. (PMID: 24098127) ; Mol Microbiol. 2008 Dec;70(6):1307-22. (PMID: 19019149) ; Hepatology. 2014 Apr;59(4):1250-61. (PMID: 23913866) ; J Biol Chem. 2017 May 5;292(18):7295-7303. (PMID: 28289095) ; J Immunol. 2012 Nov 1;189(9):4537-45. (PMID: 23008447) Grant Information: R01 AI137526 United States AI NIAID NIH HHS; R01 HL134870 United States HL NHLBI NIH HHS Contributed Indexing: Keywords: Staphylococcus aureus; VISA; host-pathogen interactions; lung; pneumonia; type I interferon; type III interferon; vancomycin Substance Nomenclature: 0 (Anti-Bacterial Agents) ; 0 (Bacterial Proteins) ; 0 (Cytokines) ; 0 (Interferon Type I) ; 0 (interferon-lambda protein, mouse) ; 6Q205EH1VU (Vancomycin) ; EC 3.4.24.75 (Lysostaphin) Entry Date(s): Date Created: 20200722 Date Completed: 20210402 Latest Revision: 20210402 Update Code: 20240513 PubMed Central ID: PMC7504949

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Differential Induction of Type I and III Interferons by Staphylococcus aureus .