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Infection and Immunity, March 2001, p. 1287-1297, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1287-1297.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Fas (CD95)-Fas Ligand Interactions Are Responsible for Monocyte Apoptosis Occurring as a Result of Phagocytosis and Killing of Staphylococcus aureus

J. Baran,1 K. Weglarczyk,2 M. Mysiak,2 K. Guzik,2 M. Ernst,3 H.-D. Flad,3 and J. Pryjma1,2,*

Department of Immunology, Polish-American Institute of Paediatrics,1 and Department of Microbiology and Immunology, Institute of Molecular Biology,2 Jagiellonian University, Cracow, Poland, and Department of Immunology and Cell Biology, Forschungszentrum Borstel, Borstel, Germany3

Received 28 June 2000/Returned for modification 6 September 2000/Accepted 27 November 2000

Human peripheral blood monocytes become apoptotic following phagocytosis of Staphylococcus aureus. In this study, we investigated the mechanisms involved in this phenomenon. Cells exposed to bacteria were examined for the surface expression of Fas and Fas ligand (FasL). The level of soluble form of FasL was also measured in the culture supernatants. As Fas-mediated apoptosis involves the activation of caspases, the activities of caspase-8 and caspase-3 were determined. Finally, the involvement of oxidative stress in apoptosis of infected monocytes was investigated. The data indicated that as a consequence of phagocytosis of S. aureus, FasL is released from the monocyte surface and induces apoptosis of phagocytic monocytes and to some extent the bystander cells. The importance of this mechanism was confirmed by demonstrating that blockage of CD95 prevents S. aureus-induced apoptosis of monocytes. Cell death occurring after phagocytosis of S. aureus involves the activation of caspase-3-like proteases, as the specific caspase-3 inhibitor suppressed apoptosis of infected cells. The generation of reactive oxygen intermediates by phagocytic monocytes by itself is not sufficient as a death signal but rather acts in up-regulating FasL shedding and possibly in modulating caspase activity.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Institute of Molecular Biology, Jagiellonian University, Al. Mickiewicza 3, 31-120 Cracow, Poland. Phone: (4812) 6341662, ext. 258. Fax: (4812) 6336907. E-mail: PRYJMA{at}mol.uj.edu.pl.

Infection and Immunity, March 2001, p. 1287-1297, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1287-1297.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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