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in Response to Bacterial Pathogens1
*
Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom;
Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen, Thailand; and
School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104
The bacterium Burkholderia pseudomallei causes a
life-threatening disease called melioidosis. In vivo experiments in
mice have identified that a rapid IFN-
response is essential for
host survival. To identify the cellular sources of IFN-, spleen
cells from uninfected mice were stimulated with B.
pseudomallei in vitro and assayed by ELISA and flow cytometry.
Costaining for intracellular IFN- vs cell surface markers
demonstrated that NK cells and, more surprisingly, CD8+ T
cells were the dominant sources of IFN-. IFN-+ NK
cells were detectable after 5 h and IFN-+
CD8+ T cells within 15 h after addition of bacteria.
IFN- production by both cell populations was inhibited by
coincubation with neutralizing mAb to IL-12 or IL-18, while a mAb to
TNF had much less effect. Three-color flow cytometry showed that
IFN--producing CD8+ T cells were of the
CD44high phenotype. The preferential activation of NK cells
and CD8+ T cells, rather than CD4+ T cells, was
also observed in response to Listeria monocytogenes or a
combination of IL-12 and IL-18 both in vitro and in vivo. This
rapid mechanism of CD8+ T cell activation may be an
important component of innate immunity to intracellular
pathogens.
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