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International Immunology Advance Access originally published online on September 26, 2005
International Immunology 2005 17(11):1409-1418; doi:10.1093/intimm/dxh319
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Schistosome larvae stimulate macrophage cytokine production through TLR4-dependent and -independent pathways

Stephen John Jenkins1,2, James Philip Hewitson1, Stephanie Ferret-Bernard1 and Adrian Paul Mountford1

1 Department of Biology, University of York, York, UK
2 Institute of Immunology and Infection Research, 101 Ashworth Laboratories, King's Buildings, University of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK

Correspondence to: S. J. Jenkins; E-mail: stephen.jenkins{at}ed.ac.uk

Exposure of the mammalian host to infective larvae of Schistosoma mansoni causes an acute inflammatory response in the skin and the activation of several cell types of the innate immune response including macrophages. Using an in vitro model of macrophage activation, we show that schistosome larvae possess molecules that directly stimulate both thioglycollate-elicited macrophages (tM{phi}) and IFN{gamma}-activated tM{phi} in vitro to produce several cytokines including IL-6, IL-12p40 and IL-10. The parasite-derived molecules are enriched within the material released by the parasite following transformation [0- to 3-h released larval preparation (0-3hRP)] but not within soluble preparations of whole larvae. Cytokine production was maintained in the presence of polymyxin B, confirming that contaminating endotoxin was not responsible. IL-12p40 and IL-10 production was much lower by cells from C3H/HeJ mice, which have defective Toll-like receptor 4 (TLR4), but IL-6 production was unaffected. Experiments using TLR4–/– mice confirmed that IL-12p40 production by tM{phi} in response to 0-3hRP was partly dependent upon functional TLR4, whereas IL-6 production was entirely independent. In contrast, tM{phi} from MyD88–/– mice failed to secrete either IL-12p40 or IL-6, underlining a pivotal role of TLR signalling in cytokine production by macrophages in response to stimulation with 0-3hRP. Finally, we show that glycan components of 0-3hRP are required for optimal cytokine production since protease treatment of 0-3hRP had no effect on IL-12p40 production and only a slight effect on IL-6, while sodium meta-periodate treatment almost completely abolished production of both cytokines.

Keywords: IL-6, IL-10, IL-12p40, innate, MyD88

Transmitting editor: A. Kelso


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