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Killing of phagocytosed Staphylococcus aureus by human neutrophils requires intracellular free calcium
Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
Department of Medical Microbiology and Immunology, University of Göteborg.
Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0002-3756-207X
Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
1996 (English)In: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 59, no 6, 902-907 p.Article in journal (Refereed) Published
Abstract [en]

The mobilization of intracellular calcium plays an important role in regulating neutrophil activation. With this in mind we investigated the effect of intra- and extracellular calcium on the ability of human neutrophils to kill complement-opsonized Staphylococcus aureus. We found that a rise in intracellular calcium is necessary for efficient killing of phagocytosed S. aureus. In the presence of extracellular calcium, killing of ingested bacteria in calcium-buffered neutrophils compared with normal cells was slightly reduced. Calcium buffering had no effect on phagocytic uptake by the neutrophils, but did decrease the generation of toxic oxygen metabolites, measured as chemiluminescence (CL). In nondepleted and calcium-depleted cells, removal of extracellular calcium did not affect ingestion but did cause a marked decrease in the ability to kill the bacteria. In parallel, the CL response was substantially reduced or completely blocked. These data show that calcium is not a prerequisite for phagocytosis of S. aureus by human neutrophils, but does play a vital role in the post-ingestion killing of the bacteria by regulating the generation of toxic oxygen metabolites.

Place, publisher, year, edition, pages
1996. Vol. 59, no 6, 902-907 p.
Keyword [en]
human leukocytes, ingestion, NADPH oxidase, respiratory burst, chemiluminescence
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-79586ISI: A1996UV31300018PubMedID: 8691076OAI: oai:DiVA.org:liu-79586DiVA: diva2:543848
Available from: 2012-08-10 Created: 2012-08-10 Last updated: 2017-12-07Bibliographically approved
In thesis
1. On the interaction between human neutrophils and Staphylococcus aureus
Open this publication in new window or tab >>On the interaction between human neutrophils and Staphylococcus aureus
2000 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Intracellular free calcium is a key second messenger and has been shown to regulate several crucial functions in human neutrophils. The results show that a rise in [Ca2+], is an absolute requirement for efficient killing of serum-opsonized Staphylococcus aureus by human neutrophils. The reduced killing in the absence of Ca2+ was not due to an inhibited ingestion of the S. aureus bacteria but to impairment of the subsequent production of oxygen radicals.

S. aureus is a bacterium which binds to extracellular matrix proteins such as vitronectin. When studying the role of Ca2+ during phagocytosis of S. aureus adherent to vitronectin-coated surfaces, the results show that a rise in [Ca2+], is not a prerequisite for ingestion per se. However, Ca2+ control neutrophil migration on vitronectin, by regulating reversible integrindependent adhesion of the neutrophils.

The intracellular signalling events of the neutrophils induced by S. aureus were also evaluated. The results demonstrate that S. aureus induces both priming and apoptosis in the neutrophils. This was restricted to viable and not heat-killed bacteria. During priming tyrosine phosphorylation of PLCγ2 and Syk is increased. In addition, the Src-family protein kinase Lyn is activated as well by these bacteria. Inhibition of these proteins by selective drugs abrogates priming of the neutrophils, indicating that these proteins participate in neutrophil priming. Interaction of neutrophils with S. aureus as well as a S. aureus-derived factor induces apoptosis in the neutrophils, and this is regulated by p38 MAPK.

Taken together, this investigation shows that the Ca2+-dependent processing of bacteria by human neutrophils leads to several cellular responses affecting inflammation, such as oxidative activation, tyrosine phosphorylation, priming and apoptosis.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2000. 60 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 634
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-28652 (URN)13808 (Local ID)91-7219-735-8 (ISBN)13808 (Archive number)13808 (OAI)
Public defence
2000-05-30, Elsa Brändströmssalen, Hälsouniversitetet, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2012-08-10Bibliographically approved

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Wilsson, ÅsaGustafsson, MikaelStendahl, Olle

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