Detection of tumor necrosis factor-α in bone marrow plasma and peripheral blood plasma from patients with aplastic anemia

1994 ◽  
Vol 45 (1) ◽  
pp. 32-38 ◽  
Author(s):  
John C. Schultz ◽  
Nasrollah T. Shahidi
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Blood Plasma ◽  
Peripheral Blood ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Bone Marrow Plasma ◽  
Peripheral Blood Plasma ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor α Stimulates Osteoclast Differentiation by a Mechanism Independent of the Odf/Rankl–Rank Interaction

2000 ◽  
Vol 191 (2) ◽  
pp. 275-286 ◽  
Author(s):  
Kanichiro Kobayashi ◽  
Naoyuki Takahashi ◽  
Eijiro Jimi ◽  
Nobuyuki Udagawa ◽  
Masamichi Takami ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Osteoclast Differentiation ◽  
Osteoclast Formation ◽  
Fab Fragment ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Osteoclast differentiation factor (ODF, also called RANKL/TRANCE/OPGL) stimulates the differentiation of osteoclast progenitors of the monocyte/macrophage lineage into osteoclasts in the presence of macrophage colony-stimulating factor (M-CSF, also called CSF-1). When mouse bone marrow cells were cultured with M-CSF, M-CSF–dependent bone marrow macrophages (M-BMMφ) appeared within 3 d. Tartrate-resistant acid phosphatase–positive osteoclasts were also formed when M-BMMφ were further cultured for 3 d with mouse tumor necrosis factor α (TNF-α) in the presence of M-CSF. Osteoclast formation induced by TNF-α was inhibited by the addition of respective antibodies against TNF receptor 1 (TNFR1) or TNFR2, but not by osteoclastogenesis inhibitory factor (OCIF, also called OPG, a decoy receptor of ODF/RANKL), nor the Fab fragment of anti–RANK (ODF/RANKL receptor) antibody. Experiments using M-BMMφ prepared from TNFR1- or TNFR2-deficient mice showed that both TNFR1- and TNFR2-induced signals were important for osteoclast formation induced by TNF-α. Osteoclasts induced by TNF-α formed resorption pits on dentine slices only in the presence of IL-1α. These results demonstrate that TNF-α stimulates osteoclast differentiation in the presence of M-CSF through a mechanism independent of the ODF/RANKL–RANK system. TNF-α together with IL-1α may play an important role in bone resorption of inflammatory bone diseases.

scholarly journals Analysis of Bone Marrow-derived Mesenchymal Stem Cell Kinetics after Short-term Stimulation with Tumor Necrosis Factor-α (TNF-α)

2019 ◽  
Vol 28 (2) ◽  
pp. 99-108 ◽  
Author(s):  
Mio Naritani ◽  
Miho Inoue ◽  
Resmi Raju ◽  
Mayu Miyagi ◽  
Masamitsu Oshima ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cell Kinetics ◽  
Short Term ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Inflammation Controls B Lymphopoiesis by Regulating Chemokine CXCL12 Expression

2004 ◽  
Vol 199 (1) ◽  
pp. 47-58 ◽  
Author(s):  
Yoshihiro Ueda ◽  
Kaiyong Yang ◽  
Sandra J. Foster ◽  
Motonari Kondo ◽  
Garnett Kelsoe
Keyword(s):  
Bone Marrow ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1 ◽  
B Lymphopoiesis ◽  
Cxcl12 Expression ◽  
Chemokine Cxcl12 ◽  
Factor Α ◽  
Necrosis Factor

Inflammation removes developing and mature lymphocytes from the bone marrow (BM) and induces the appearance of developing B cells in the spleen. BM granulocyte numbers increase after lymphocyte reductions to support a reactive granulocytosis. Here, we demonstrate that inflammation, acting primarily through tumor necrosis factor α (TNFα), mobilizes BM lymphocytes. Mobilization reflects a reduced CXCL12 message and protein in BM and changes to the BM environment that prevents homing by cells from naive donors. The effects of TNFα are potentiated by interleukin 1 β (IL-1β), which acts primarily to expand the BM granulocyte compartment. Our observations indicate that inflammation induces lymphocyte mobilization by suppressing CXCL12 retention signals in BM, which, in turn, increases the ability of IL-1β to expand the BM granulocyte compartment. Consistent with this idea, lymphocyte mobilization and a modest expansion of BM granulocyte numbers follow injections of pertussis toxin. We propose that TNFα and IL-1β transiently specialize the BM to support acute granulocytic responses and consequently promote extramedullary lymphopoiesis.

Tumor Necrosis Factor-α in the Placenta is not Elevated in Pre-eclamptic Patients Despite its Elevation in Peripheral Blood

2005 ◽  
Vol 53 (3) ◽  
pp. 113-119 ◽  
Author(s):  
Masatoshi Hayashi ◽  
Yoshihiko Ueda ◽  
Takehiko Yamaguchi ◽  
Ryoichi Sohma ◽  
Mitsuei Shibazaki ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Peripheral Blood ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor
Sign in / Sign up

Export Citation Format

Share Document