Heat shock protein 60 causes osteoclastic bone resorption via toll-like receptor-2 in estrogen deficiency

Bone ◽  
2009 ◽  
Vol 45 (4) ◽  
pp. 650-660 ◽  
Author(s):  
Jung-Min Koh ◽  
Young-Sun Lee ◽  
Yang Soon Kim ◽  
Su-Hye Park ◽  
Seung Hun Lee ◽  
...  
Keyword(s):  
Heat Shock ◽  
Bone Resorption ◽  
Heat Shock Protein ◽  
Estrogen Deficiency ◽  
Osteoclastic Bone Resorption ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Heat shock protein 60 fromChlamydia pneumoniae elicits an unusual set of inflammatory responses via Toll-like receptor 2 and 4in vivo

2004 ◽  
Vol 34 (10) ◽  
pp. 2874-2884 ◽  
Author(s):  
Clarissa U. Prazeres da Costa ◽  
Nina Wantia ◽  
Carsten J. Kirschning ◽  
Dirk H. Busch ◽  
Nuria Rodriguez ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Inflammatory Responses ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Detrimental Role of Heat Shock Protein 60&70 and Toll-like Receptor 4 in Skeletal Muscle Ischaemia In Vitro

2013 ◽  
Vol 57 (5) ◽  
pp. 77S
Author(s):  
Ali Navi ◽  
Rebekah Yu ◽  
Xu Shi-Wen ◽  
Sidney Shaw ◽  
George Hamilton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 60 ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Muscle Ischaemia

scholarly journals The Endoplasmic Reticulum-resident Heat Shock Protein Gp96 Activates Dendritic Cells via the Toll-like Receptor 2/4 Pathway

2002 ◽  
Vol 277 (23) ◽  
pp. 20847-20853 ◽  
Author(s):  
Ramunas M. Vabulas ◽  
Sibylla Braedel ◽  
Norbert Hilf ◽  
Harpreet Singh-Jasuja ◽  
Sylvia Herter ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Dendritic Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Toll Like Receptor ◽  
Heat Shock Protein Gp96 ◽  
Toll Like Receptor 2

70kDa heat shock protein is an endogenous Toll-Like receptor 2 inducer in mid-trimester amniotic fluid

2005 ◽  
Vol 193 (6) ◽  
pp. S32
Author(s):  
Claudel Jean-Pierre (F) ◽  
Sriram C. Perni ◽  
Robin B. Kalish ◽  
Ann Marie Bongiovanni ◽  
Emerie Karasahan ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Amniotic Fluid ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Helicobacter pylori heat-shock protein 60 induces interleukin-8 via a Toll-like receptor (TLR)2 and mitogen-activated protein (MAP) kinase pathway in human monocytes

2007 ◽  
Vol 56 (2) ◽  
pp. 154-164 ◽  
Author(s):  
Ying Zhao ◽  
Kenji Yokota ◽  
Kiyoshi Ayada ◽  
Yumiko Yamamoto ◽  
Tomayuki Okada ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
P38 Mapk ◽  
Heat Shock Protein 60 ◽  
Human Monocytes ◽  
Toll Like Receptor ◽  
Mapk Signalling ◽  
Mitogen Activated Protein ◽  
H Pylori

Previous reports have indicated that Helicobacter pylori heat-shock protein 60 (H. pylori-HSP60), as an immunodominant antigen, induces interleukin (IL)-8 production in human monocytes. The exact mechanism by which H. pylori-HSP60 induces IL-8 production in monocytes has not been fully elucidated. In the present study, the downstream pathway by which H. pylori-HSP60 induces IL-8 secretion in human monocytic cell lines was investigated. Intact H. pylori, heat-killed H. pylori and H. pylori recombinant HSP60 (rHpHSP60) all induced the secretion of IL-8 and the activation of mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) and p38, but not c-Jun N-terminal kinase (JNK), up to 24 h in NOMO1 cells. The specific inhibitors PD98059 and U0126 (for ERK1/2 signalling) and SB203580 (for p38 MAPK signalling) down-regulated IL-8 secretion from rHpHSP60-treated NOMO1 cells. An anti-Toll-like receptor (TLR)2 antibody or TLR2 small interfering RNA (siRNA) partially inhibited the secretion of IL-8, and anti-TLR2 antibody also suppressed activation of ERK and p38 MAPK in rHpHSP60-treated NOMO1 cells. These reactions were associated with nuclear factor-κB (NF-κB)-mediated transcriptional activation, since U0126, SB203580 and the anti-TLR2 antibody decreased NF-κB activation. Taken together, the results suggest that ERK and p38 MAPK signalling linked to the TLR2 recognition receptor in human monocytes may be an important pathway in H. pylori-HSP60-induced IL-8 secretion.

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