Staphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake.

2.50
Hdl Handle:
http://hdl.handle.net/10033/214669
Title:
Staphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake.
Authors:
Abel, Jens; Goldmann, Oliver; Ziegler, Christina; Höltje, Claudia; Smeltzer, Mark S; Cheung, Ambrose L; Bruhn, Daniela; Rohde, Manfred; Medina, Eva
Abstract:
In this study, we investigated the interactions of Staphylococcus aureus with mast cells, which are multifunctional sentinels lining the surfaces of the body. We found that bone marrow-derived murine mast cells (BMMC) exerted a powerful phagocytosis-independent antimicrobial activity against S. aureus. Both the release of extracellular traps as well as discharge of antimicrobial compounds were the mechanisms used by the BMMC to kill extracellular S. aureus. This was accompanied by the secretion of mediators such as TNF-α involved in the recruitment of effector cells. Interestingly, S. aureus subverted the extracellular antimicrobial activity of the BMMC by internalizing within these cells. S. aureus was also capable to internalize within human mast cells (HMC-1) and within murine skin mast cells during in vivo infection. Bacteria internalization was, at least in part, mediated by the α5β1 integrins expressed on the surface of the mast cell. In the intracellular milieu, the bacterium survived and persisted by increasing the cell wall thickness and by gaining access into the mast cell cytosol. The expression of α-hemolysin was essential for staphylococci intracellular persistence. By hiding within the long-life mast cells, staphylococci not only avoid clearance but also establish an infection reservoir that could contribute to chronic carriage.
Affiliation:
Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Citation:
Staphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake. 2011, 3 (5):495-507 J Innate Immun
Journal:
Journal of innate immunity
Issue Date:
2011
URI:
http://hdl.handle.net/10033/214669
DOI:
10.1159/000327714
PubMed ID:
21654154
Type:
Article
Language:
en
ISSN:
1662-8128
Appears in Collections:
Publications of RG Infection Immunology (INI)

Full metadata record

DC FieldValue Language
dc.contributor.authorAbel, Jensen
dc.contributor.authorGoldmann, Oliveren
dc.contributor.authorZiegler, Christinaen
dc.contributor.authorHöltje, Claudiaen
dc.contributor.authorSmeltzer, Mark Sen
dc.contributor.authorCheung, Ambrose Len
dc.contributor.authorBruhn, Danielaen
dc.contributor.authorRohde, Manfreden
dc.contributor.authorMedina, Evaen
dc.date.accessioned2012-03-07T15:14:34Z-
dc.date.available2012-03-07T15:14:34Z-
dc.date.issued2011-
dc.identifier.citationStaphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake. 2011, 3 (5):495-507 J Innate Immunen
dc.identifier.issn1662-8128-
dc.identifier.pmid21654154-
dc.identifier.doi10.1159/000327714-
dc.identifier.urihttp://hdl.handle.net/10033/214669-
dc.description.abstractIn this study, we investigated the interactions of Staphylococcus aureus with mast cells, which are multifunctional sentinels lining the surfaces of the body. We found that bone marrow-derived murine mast cells (BMMC) exerted a powerful phagocytosis-independent antimicrobial activity against S. aureus. Both the release of extracellular traps as well as discharge of antimicrobial compounds were the mechanisms used by the BMMC to kill extracellular S. aureus. This was accompanied by the secretion of mediators such as TNF-α involved in the recruitment of effector cells. Interestingly, S. aureus subverted the extracellular antimicrobial activity of the BMMC by internalizing within these cells. S. aureus was also capable to internalize within human mast cells (HMC-1) and within murine skin mast cells during in vivo infection. Bacteria internalization was, at least in part, mediated by the α5β1 integrins expressed on the surface of the mast cell. In the intracellular milieu, the bacterium survived and persisted by increasing the cell wall thickness and by gaining access into the mast cell cytosol. The expression of α-hemolysin was essential for staphylococci intracellular persistence. By hiding within the long-life mast cells, staphylococci not only avoid clearance but also establish an infection reservoir that could contribute to chronic carriage.en
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshApoptosisen
dc.subject.meshBacterial Toxinsen
dc.subject.meshCarrier Stateen
dc.subject.meshCell Lineen
dc.subject.meshCytotoxicity, Immunologicen
dc.subject.meshDisease Reservoirsen
dc.subject.meshEndocytosisen
dc.subject.meshHemolysin Proteinsen
dc.subject.meshHost-Pathogen Interactionsen
dc.subject.meshHumansen
dc.subject.meshImmune Evasionen
dc.subject.meshIntegrin alpha5beta1en
dc.subject.meshMast Cellsen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshStaphylococcal Infectionsen
dc.subject.meshStaphylococcus aureusen
dc.subject.meshTumor Necrosis Factor-alphaen
dc.titleStaphylococcus aureus evades the extracellular antimicrobial activity of mast cells by promoting its own uptake.en
dc.typeArticleen
dc.contributor.departmentInfection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.en
dc.identifier.journalJournal of innate immunityen

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