Inhibitory Effects of Tumor Necrosis Factor-Alpha on Migration of Human Periodontal Ligament Cells

2006 ◽  
Vol 77 (5) ◽  
pp. 883-890 ◽  
Author(s):  
Akane Takemura ◽  
Ichiro Nakagawa ◽  
Shinji Kawai ◽  
Hiroaki Inaba ◽  
Takahiro Kato ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Periodontal Ligament ◽  
Tumor Necrosis ◽  
Periodontal Ligament Cells ◽  
Inhibitory Effects ◽  
Necrosis Factor Alpha ◽  
Human Periodontal Ligament Cells ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Potentiation of early hematopoiesis by tumor necrosis factor-alpha is followed by inhibition of granulopoietic differentiation and proliferation

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 635-644 ◽  
Author(s):  
C Caux ◽  
C Favre ◽  
S Saeland ◽  
V Duvert ◽  
I Durand ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Inhibitory Effects ◽  
Granulocytic Differentiation ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Differentiation And Proliferation ◽  
Necrosis Factor

We have previously shown that tumor necrosis factor-alpha (TNF alpha) strongly potentiates interleukin-3 (IL-3)-induced short-term proliferation of human CD34+ hematopoietic progenitor cells (HPC). Using longer term cultures of CD34+ HPC, we demonstrate here that this initial potentiation ceases after 10 to 12 days; whereupon TNF alpha displays inhibitory effects. Thus, TNF alpha was found to inhibit cells of granulocytic affiliation while it potentiates the development of maturing cells of the monocytic lineage both in liquid and semi-solid (day 14 colony-forming unit) cultures. TNF alpha was demonstrated to reversibly block granulocytic differentiation at the level of uncommitted CD13-, CD15- blast cells that accumulate in IL-3 + TNF alpha cultures. Furthermore, growth of committed granulocytes (CD15+) from IL-3 cultures was also inhibited by TNF alpha through an arrest of cell cycle in G0/G1. Finally, the use of neutralizing anti-TNF alpha monoclonal antibody and limiting dilution studies indicate that the inhibitory effects of TNF alpha are direct. Taken together, our data demonstrate that, following a phase of potentiation of proliferation of early HPC, TNF alpha displays direct inhibitory effects due to negative interference with both granulocytic differentiation and proliferation of granulocytic cells.

Inhibitory effects of tumor necrosis factor alpha on fracture healing in rats

Bone ◽  
1989 ◽  
Vol 10 (6) ◽  
pp. 453-457 ◽  
Author(s):  
J. Hashimoto ◽  
H. Yoshikawa ◽  
K. Takaoka ◽  
N. Shimizu ◽  
K. Masuhara ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Fracture Healing ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inhibitory Effects ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Toxoplasma gondii Inhibits Toll-Like Receptor 4 Ligand-Induced Mobilization of Intracellular Tumor Necrosis Factor Alpha to the Surface of Mouse Peritoneal Neutrophils

2006 ◽  
Vol 74 (7) ◽  
pp. 4274-4281 ◽  
Author(s):  
Soumaya Bennouna ◽  
Woraporn Sukhumavasi ◽  
Eric Y. Denkers
Keyword(s):  
Toxoplasma Gondii ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Toll Like Receptor ◽  
Inhibitory Effects ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Neutrophils are well-known to rapidly respond to infection through chemotactic infiltration at sites of inflammation, followed by rapid release of microbicidal molecules, chemokines, and proinflammatory cytokines. For tumor necrosis factor alpha (TNF-α), we recently found that neutrophils contain intracellular pools of the cytokine and display the capacity to upregulate transcriptional activity of the gene during lipopolysaccharide (LPS) stimulation. We now show that triggering of mouse peritoneal neutrophils with Toll-like receptor 2 (TLR2), TLR4, and TLR9 ligands, but not ligands of TLR3, induces upregulation of surface membrane TNF-α. However, neutrophils infected with the protozoan Toxoplasma gondii displayed an inability to respond fully in terms of TLR ligand-induced increases in membrane TNF-α expression. Infected neutrophils failed to display decreased levels of intracellular TNF-α upon LPS exposure. In contrast to intermediate inhibitory effects in nontreated neutrophils, T. gondii induced a complete blockade in LPS-induced surface TNF-α expression in the presence of the protein synthesis inhibitor cycloheximide. Despite these inhibitory effects, the parasite did not affect LPS-induced upregulation of TNF-α gene transcription. Collectively, the results show that Toxoplasma prevents TLR ligand-triggered mobilization of TNF-α to the neutrophil surface, revealing a novel immunosuppressive activity of the parasite.

scholarly journals Potentiation of early hematopoiesis by tumor necrosis factor-alpha is followed by inhibition of granulopoietic differentiation and proliferation

Blood ◽  
1991 ◽  
Vol 78 (3) ◽  
pp. 635-644 ◽  
Author(s):  
C Caux ◽  
C Favre ◽  
S Saeland ◽  
V Duvert ◽  
I Durand ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Inhibitory Effects ◽  
Granulocytic Differentiation ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Differentiation And Proliferation ◽  
Necrosis Factor

Abstract We have previously shown that tumor necrosis factor-alpha (TNF alpha) strongly potentiates interleukin-3 (IL-3)-induced short-term proliferation of human CD34+ hematopoietic progenitor cells (HPC). Using longer term cultures of CD34+ HPC, we demonstrate here that this initial potentiation ceases after 10 to 12 days; whereupon TNF alpha displays inhibitory effects. Thus, TNF alpha was found to inhibit cells of granulocytic affiliation while it potentiates the development of maturing cells of the monocytic lineage both in liquid and semi-solid (day 14 colony-forming unit) cultures. TNF alpha was demonstrated to reversibly block granulocytic differentiation at the level of uncommitted CD13-, CD15- blast cells that accumulate in IL-3 + TNF alpha cultures. Furthermore, growth of committed granulocytes (CD15+) from IL-3 cultures was also inhibited by TNF alpha through an arrest of cell cycle in G0/G1. Finally, the use of neutralizing anti-TNF alpha monoclonal antibody and limiting dilution studies indicate that the inhibitory effects of TNF alpha are direct. Taken together, our data demonstrate that, following a phase of potentiation of proliferation of early HPC, TNF alpha displays direct inhibitory effects due to negative interference with both granulocytic differentiation and proliferation of granulocytic cells.

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