Distinct Roles for MyD88 and Toll-Like Receptors 2, 5, and 9 in Phagocytosis ofBorrelia burgdorferiand Cytokine Induction

• DOI: 10.1128/iai.01600-07
• Publication Date: 2008-04-01T00:45:18Z
• Authors: Ok S. Shin; Ralph R. Isberg; Shizuo Akira; Satoshi Uematsu; Aruna K. Behera; Linden T. Hu
• Keywords: Inflammation; Mice, Knockout; 0301 basic medicine; 0303 health sciences; Lipoproteins; Macrophages; p38 Mitogen-Activated Protein Kinases; Toll-Like Receptor 2; Cell Line; Mice; Toll-Like Receptor 5; 03 medical and health sciences; Bacterial Proteins; Gene Expression Regulation; Phagocytosis; Borrelia burgdorferi; Toll-Like Receptor 9; Myeloid Differentiation Factor 88; Animals; Cytokines; RNA Interference; RNA, Small Interfering; Signal Transduction

ABSTRACT The contribution of Toll-like receptors (TLRs) to phagocytosis Borrelia burgdorferi has not been extensively studied. We show that bone marrow-derived macrophages (BMDM) from MyD88 −/− mice or Raw cells transfected with a dominant-negative were unable efficiently internalize B. burgdorferi. Knockouts TLR2 and TLR9 knockdown TLR5 by small interfering RNA produced no defects in . Production inflammatory cytokines was greatly diminished BMDM but only partially affected unaffected BMDM. Cytochalasin D reduced cytokine induction, the level Addition cytochalasin inhibited responses BMDM, consistent role for both recognition extracellular products lysosomal sampling after processing organism. had impact on production undergoing knockdown. These results suggest MyD88, TLR2, TLR5, TLR9, is important uptake affects through its effects transducing signals TLR5.