Staphylococcus aureus Evades the Extracellular Antimicrobial Activity of Mast Cells by Promoting Its Own UptakeAbel J.a · Goldmann O.a · Ziegler C.a · Höltje C.a · Smeltzer M.S.c · Cheung A.L.d · Bruhn D.a · Rohde M.b · Medina E.a
aInfection Immunology Research Group and bDepartment of Medical Microbiology, Helmholtz Centre for Infection Research, Braunschweig, Germany; cDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Ark., and dDepartment of Microbiology, Dartmouth Medical School, Hanover, N.H., USA.
Dr. Eva Medina
Infection Immunology Research Group
Helmholtz Centre for Infection Research, Inhoffenstrasse 7
DE–38124 Braunschweig (Germany)
Tel. +49 531 6181 4500, E-Mail firstname.lastname@example.org
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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.
© 2011 S. Karger AG, Basel
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