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* Department of Internal Medicine, Division of Nephrology and
Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University Graduate School of Medicine, Nagoya, Japan;
Toyama Institute of Health, Toyama, Japan; and
Department of Host Defense, Research Institute for Microbial Disease, Osaka University, Osaka, Japan
Pyelonephritis, in which renal tubular epithelial cells are
directly exposed to bacterial component, is a major predisposing cause
of renal insufficiency. Although previous studies have suggested C-C
chemokines are involved in the pathogenesis, the exact source and
mechanisms of the chemokine secretion remain ambiguous. In this study,
we evaluated the involvement of Toll-like receptors (TLRs) in C-C
chemokine production by mouse primary renal tubular epithelial cells
(MTECs). MTECs constitutively expressed mRNA for TLR1, 2, 3, 4, and 6,
but not for TLR5 or 9. MTECs also expressed MD-2, CD14, myeloid
differentiation factor 88, and Toll receptor-IL-1R domain-containing
adapter protein/myeloid differentiation factor 88-adapter-like.
Synthetic lipid A and lipoprotein induced monocyte chemoattractant
protein 1 (MCP-1) and RANTES production in MTECs, which strictly depend
on TLR4 and TLR2, respectively. In contrast, MTECs were refractory to
CpG-oligodeoxynucleotide in chemokine production, consistently with the
absence of TLR9. LPS-mediated MCP-1 and RANTES production in MTECs was
abolished by NF-
B inhibition, but unaffected by extracellular
signal-regulated kinase inhibition. In LPS-stimulated MTECs, inhibition
of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase
significantly decreased RANTES, but did not affect MCP-1 mRNA
induction. Thus, MTECs have a distinct expression pattern of TLR and
secrete C-C chemokines in response to direct stimulation with a set of
bacterial components.
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