Bacterial Lipoproteins Constitute the TLR2-Stimulating Activity of Serum Amyloid A.

Autor:	Burgess EJ; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Hoyt LR; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Randall MJ; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Mank MM; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Bivona JJ 3rd; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Eisenhauer PL; Immunobiology Division, Department of Medicine, University of Vermont, Burlington, VT 05405., Botten JW; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Immunobiology Division, Department of Medicine, University of Vermont, Burlington, VT 05405.; Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405., Ballif BA; Department of Biology, University of Vermont, Burlington, VT 05405; and., Lam YW; Department of Biology, University of Vermont, Burlington, VT 05405; and., Wargo MJ; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405., Boyson JE; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Department of Surgery, University of Vermont, Burlington, VT 05405., Ather JL; Vermont Lung Center, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405., Poynter ME; Vermont Lung Center, University of Vermont, Burlington, VT 05405; matthew.poynter@med.uvm.edu.; Cellular, Molecular, and Biomedical Sciences Program, University of Vermont, Burlington, VT 05405.; Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT 05405.
Jazyk:	angličtina
Zdroj:	Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2018 Oct 15; Vol. 201 (8), pp. 2377-2384. Date of Electronic Publication: 2018 Aug 29.
DOI:	10.4049/jimmunol.1800503
Abstrakt:	Studies comparing endogenous and recombinant serum amyloid A (SAA) have generated conflicting data on the proinflammatory function of these proteins. In exploring this discrepancy, we found that in contrast to commercially sourced recombinant human SAA1 (hSAA1) proteins produced in Escherichia coli , hSAA1 produced from eukaryotic cells did not promote proinflammatory cytokine production from human or mouse cells, induce Th17 differentiation, or stimulate TLR2. Proteomic analysis of E. coli -derived hSAA1 revealed the presence of numerous bacterial proteins, with several being reported or probable lipoproteins. Treatment of hSAA1 with lipoprotein lipase or addition of a lipopeptide to eukaryotic cell-derived hSAA1 inhibited or induced the production of TNF-α from macrophages, respectively. Our results suggest that a function of SAA is in the binding of TLR2-stimulating bacterial proteins, including lipoproteins, and demand that future studies of SAA employ a recombinant protein derived from eukaryotic cells. (Copyright © 2018 by The American Association of Immunologists, Inc.)
Databáze:	MEDLINE
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