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Title

The proinflammatory cytokine response to Chlamydia trachomatis elementary bodies in human macrophages is partly mediated by a lipoprotein, the macrophage infectivity potentiator, through TLR2/TLR1/TLR6 and CD14

Authors
Vuillet, Madeleine
Seya, Tsukasa
Matsumoto, Misako
Published in Journal of Immunology. 2008, vol. 180, no. 2, p. 1158-68
Abstract Chlamydiae components and signaling pathway(s) responsible for the production of proinflammatory cytokines by human monocytes/macrophages are not clearly identified. To this aim, Chlamydia trachomatis-inactivated elementary bodies (EB) as well as the following seven individual Ags were tested for their ability to induce the production of proinflammatory cytokines by human monocytes/macrophages and THP-1 cells: purified LPS, recombinant heat shock protein (rhsp)70, rhsp60, rhsp10, recombinant polypeptide encoded by open reading frame 3 of the plasmid (rpgp3), recombinant macrophage infectivity potentiator (rMip), and recombinant outer membrane protein 2 (rOmp2). Aside from EB, rMip displayed the highest ability to induce release of IL-1beta, TNF-alpha, IL-6, and IL-8. rMip proinflammatory activity could not be attributed to Escherichia coli LPS contamination as determined by the Limulus Amoebocyte lysate assay, insensitivity to polymyxin B (50 microg/ml), and different serum requirement. We have recently demonstrated that Mip is a "classical" bacterial lipoprotein, exposed at the surface of EB. The proinflammatory activity of EB was significantly attenuated in the presence of polyclonal Ab to rMip. Native Mip was able to induce TNF-alpha and IL-8 secretion, whereas a nonlipidated C20A rMip variant was not. Proinflammatory activity of rMip was unaffected by heat or proteinase K treatments but was greatly reduced by treatment with lipases, supporting a role of lipid modification in this process. Stimulating pathways appeared to involve TLR2/TLR1/TLR6 with the help of CD14 but not TLR4. These data support a role of Mip lipoprotein in pathogenesis of C. trachomatis-induced inflammatory responses.
Keywords Antibodies/pharmacologyAntibodies Bacterial/pharmacologyAntigens CD14/immunology/metabolismBacterial Proteins/antagonists & inhibitors/immunologyChlamydia Infections/immunologyChlamydia trachomatis/immunologyCytokines/antagonists & inhibitors/metabolismEscherichia coli/immunologyHumansImmunoglobulin G/pharmacologyLipopolysaccharides/immunologyLipoproteins/antagonists & inhibitors/immunologyMacrophagesToll-Like Receptor 1/antagonists & inhibitors/metabolismToll-Like Receptor 2/antagonists & inhibitors/metabolismToll-Like Receptor 6/antagonists & inhibitors/metabolismTumor Necrosis Factor-alpha/antagonists & inhibitors/metabolism
Identifiers
PMID: 18178856
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Other version: http://www.jimmunol.org/cgi/content/full/180/2/1158
Structures
Research group Mécanisme de l'inflammation articulaire (44)
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(ISO format)
BAS, Sylvette et al. The proinflammatory cytokine response to Chlamydia trachomatis elementary bodies in human macrophages is partly mediated by a lipoprotein, the macrophage infectivity potentiator, through TLR2/TLR1/TLR6 and CD14. In: Journal of Immunology, 2008, vol. 180, n° 2, p. 1158-68. doi: 10.4049/jimmunol.180.2.1158 https://archive-ouverte.unige.ch/unige:781

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Deposited on : 2009-02-12

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