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Infection and Immunity, January 2000, p. 320-327, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Intracellular and Extracellular Cytokine Production by Human Mixed Mononuclear Cells in Response to Group B Streptococci

Daniel J. Kwak,1 Nancy H. Augustine,2 Wellington G. Borges,3 Joanna L. Joyner,2 Wayne F. Green,4,5 and Harry R. Hill1,2,5,*

Departments of Pathology,2 Pediatrics,1 and Internal Medicine5 and the Huntsman Cancer Institute,4 University of Utah School of Medicine, Salt Lake City, Utah 84132, and the Department of Pediatrics, Hospital de Base de Brasilia, Brasilia D.F., Brazil3

Received 1 July 1999/Returned for modification 8 September 1999/Accepted 11 October 1999

Group B streptococci (GBS) are a major cause of severe infection in newborns, pregnant females, and other immunocompromised hosts. Infection often includes septicemia, shock, pneumonia, and respiratory failure. In previous studies, we have reported that GBS induce marked production of tumor necrosis factor alpha (TNF-alpha ) by human mononuclear cells. The present study was designed to measure the production of TNF-alpha as well as additional cytokines, including interleukin 1beta (IL-1beta ), IL-6, IL-8, IL-12, and gamma interferon (IFN-gamma ) but also to determine from what cells and at what time point during incubation with GBS that these cytokines are produced. Mixed mononuclear cells were incubated with heat-killed GBS, media alone, or 1 µg of Escherichia coli lipopolysaccharide (LPS). Brefeldin A was added to each sample prior to staining, which prevented the export of cytokines by the Golgi apparatus. The cells were then stained with the appropriate conjugated antibodies and analyzed by using a flow cytometer. Results indicate that intracellular cytokines appear, in almost all cases, simultaneous to or before secreted proteins are detected. In contrast to the response to LPS, where TNF-alpha , IL-1beta , IL-6, and IL-8 appear almost simultaneously, the human monocyte response to GBS results in the production of TNF-alpha but delayed appearance of IL-1beta , IL-6, and IL-8. The lymphocyte response to GBS was also strikingly different from that to LPS in that both secreted IFN-gamma and IL-12 was detected, while LPS failed to induce production of these critical cytokines. This suggests an important role for TNF-alpha , IFN-gamma , and IL-12 in GBS pathogenesis and/or immunity.

* Corresponding author. Mailing address: Department of Pathology, University of Utah School of Medicine, 50 North Medical Dr., Salt Lake City, UT 84132. Phone: (801) 581-5873. Fax: (801) 585-1265. E-mail: Harry.Hill{at}path.med.utah.edu.

Infection and Immunity, January 2000, p. 320-327, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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