MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α

MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α

Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin (IL)-1 receptor family. Toll–IL-1 receptor domain-containing adaptor inducing interferon-β (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Usi...

Full description

Bibliographic Details
Main Authors: Sato, Nobuaki, Takahashi, Naoyuki, Suda, Koji, Nakamura, Midori, Yamaki, Mariko, Ninomiya, Tadashi, Kobayashi, Yasuhiro, Takada, Haruhiko, Shibata, Kenichiro, Yamamoto, Masahiro, Takeda, Kiyoshi, Akira, Shizuo, Noguchi, Toshihide, Udagawa, Nobuyuki
Format: Online
Language:English
Published: The Rockefeller University Press 2004
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212746/
id pubmed-2212746
recordtype oai_dc
spelling pubmed-22127462008-03-11 MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α Sato, Nobuaki Takahashi, Naoyuki Suda, Koji Nakamura, Midori Yamaki, Mariko Ninomiya, Tadashi Kobayashi, Yasuhiro Takada, Haruhiko Shibata, Kenichiro Yamamoto, Masahiro Takeda, Kiyoshi Akira, Shizuo Noguchi, Toshihide Udagawa, Nobuyuki Article Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin (IL)-1 receptor family. Toll–IL-1 receptor domain-containing adaptor inducing interferon-β (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Using MyD88-deficient (MyD88−/−) mice and TRIF-deficient (TRIF−/−) mice, we examined roles of MyD88 and TRIF in osteoclast differentiation and function. LPS, diacyl lipopeptide, and IL-1α stimulated osteoclastogenesis in cocultures of osteoblasts and hemopoietic cells obtained from TRIF−/− mice, but not MyD88−/− mice. These factors stimulated receptor activator of nuclear factor-κB ligand mRNA expression in TRIF−/− osteoblasts, but not MyD88−/− osteoblasts. LPS stimulated IL-6 production in TRIF−/− osteoblasts, but not TRIF−/− macrophages. LPS and IL-1α enhanced the survival of TRIF−/− osteoclasts, but not MyD88−/− osteoclasts. Diacyl lipopeptide did not support the survival of osteoclasts because of the lack of Toll-like receptor (TLR)6 in osteoclasts. Macrophages expressed both TRIF and TRIF-related adaptor molecule (TRAM) mRNA, whereas osteoblasts and osteoclasts expressed only TRIF mRNA. Bone histomorphometry showed that MyD88−/− mice exhibited osteopenia with reduced bone resorption and formation. These results suggest that the MyD88-mediated signal is essential for the osteoclastogenesis and function induced by IL-1 and TLR ligands, and that MyD88 is physiologically involved in bone turnover. The Rockefeller University Press 2004-09-06 /pmc/articles/PMC2212746/ /pubmed/15353553 http://dx.doi.org/10.1084/jem.20040689 Text en Copyright © 2004, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Sato, Nobuaki
Takahashi, Naoyuki
Suda, Koji
Nakamura, Midori
Yamaki, Mariko
Ninomiya, Tadashi
Kobayashi, Yasuhiro
Takada, Haruhiko
Shibata, Kenichiro
Yamamoto, Masahiro
Takeda, Kiyoshi
Akira, Shizuo
Noguchi, Toshihide
Udagawa, Nobuyuki
spellingShingle Sato, Nobuaki
Takahashi, Naoyuki
Suda, Koji
Nakamura, Midori
Yamaki, Mariko
Ninomiya, Tadashi
Kobayashi, Yasuhiro
Takada, Haruhiko
Shibata, Kenichiro
Yamamoto, Masahiro
Takeda, Kiyoshi
Akira, Shizuo
Noguchi, Toshihide
Udagawa, Nobuyuki
MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
author_facet Sato, Nobuaki
Takahashi, Naoyuki
Suda, Koji
Nakamura, Midori
Yamaki, Mariko
Ninomiya, Tadashi
Kobayashi, Yasuhiro
Takada, Haruhiko
Shibata, Kenichiro
Yamamoto, Masahiro
Takeda, Kiyoshi
Akira, Shizuo
Noguchi, Toshihide
Udagawa, Nobuyuki
author_sort Sato, Nobuaki
title MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
title_short MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
title_full MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
title_fullStr MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
title_full_unstemmed MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α
title_sort myd88 but not trif is essential for osteoclastogenesis induced by lipopolysaccharide, diacyl lipopeptide, and il-1α
description Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin (IL)-1 receptor family. Toll–IL-1 receptor domain-containing adaptor inducing interferon-β (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Using MyD88-deficient (MyD88−/−) mice and TRIF-deficient (TRIF−/−) mice, we examined roles of MyD88 and TRIF in osteoclast differentiation and function. LPS, diacyl lipopeptide, and IL-1α stimulated osteoclastogenesis in cocultures of osteoblasts and hemopoietic cells obtained from TRIF−/− mice, but not MyD88−/− mice. These factors stimulated receptor activator of nuclear factor-κB ligand mRNA expression in TRIF−/− osteoblasts, but not MyD88−/− osteoblasts. LPS stimulated IL-6 production in TRIF−/− osteoblasts, but not TRIF−/− macrophages. LPS and IL-1α enhanced the survival of TRIF−/− osteoclasts, but not MyD88−/− osteoclasts. Diacyl lipopeptide did not support the survival of osteoclasts because of the lack of Toll-like receptor (TLR)6 in osteoclasts. Macrophages expressed both TRIF and TRIF-related adaptor molecule (TRAM) mRNA, whereas osteoblasts and osteoclasts expressed only TRIF mRNA. Bone histomorphometry showed that MyD88−/− mice exhibited osteopenia with reduced bone resorption and formation. These results suggest that the MyD88-mediated signal is essential for the osteoclastogenesis and function induced by IL-1 and TLR ligands, and that MyD88 is physiologically involved in bone turnover.
publisher The Rockefeller University Press
publishDate 2004
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212746/
_version_ 1611434350959656960

Similar Items