Lipoxin A4 and aspirin-triggered 15-epi-LXA4 inhibit tumor necrosis factor-alpha-initiated neutrophil responses and trafficking: novel regulators of a cytokine-chemokine axis relevant to periodontal diseases

1999 ◽  
Vol 34 (7) ◽  
pp. 370-373 ◽  
Author(s):  
Marc Pouliot ◽  
Charles N. Serhan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Periodontal Diseases ◽  
Lipoxin A4 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Inhibit Tumor Necrosis Factor

scholarly journals Filifactor alocis and Tumor Necrosis Factor-Alpha Stimulate Synthesis of Visfatin by Human Macrophages

2021 ◽  
Vol 22 (3) ◽  
pp. 1235
Author(s):  
Andressa Vilas Boas Nogueira ◽  
Marjan Nokhbehsaim ◽  
Anna Damanaki ◽  
Sigrun Eick ◽  
Christian Kirschneck ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Periodontal Diseases ◽  
Immune Defense ◽  
Necrosis Factor Alpha ◽  
Human Macrophages ◽  
Factor Alpha ◽  
Filifactor Alocis ◽  
Necrosis Factor

There is little known about the effect of the periodontopathogen Filifactor alocis on macrophages as key cells of the innate immune defense in the periodontium. Therefore, the aim of the present study was to investigate the effect of F. alocis and additionally of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) on visfatin and other pro-inflammatory and proteolytic molecules associated with periodontitis in human macrophages. The presence of macrophage markers CD14, CD86, CD68, and CD163 was examined in gingival biopsies from healthy individuals and periodontitis patients. Human macrophages were incubated with F. alocis and TNFα for up to 2 d. The effects of both stimulants on macrophages were determined by real-time PCR, ELISA, immunocytochemistry, and immunofluorescence. F. alocis was able to significantly stimulate the synthesis of visfatin by human macrophages using TLR2 and MAPK pathways. In addition to visfatin, F. alocis was also able to increase the synthesis of cyclooxygenase 2, TNFα, and matrix metalloproteinase 1. Like F. alocis, TNFα was also able to stimulate the production of these proinflammatory and proteolytic molecules. Our results highlight the pathogenetic role of F. alocis in periodontal diseases and also underline the involvement of visfatin in the aetiopathogenesis of periodontitis.

Docosahexaenoic acid-enriched phospholipids and eicosapentaenoic acid-enriched phospholipids inhibit tumor necrosis factor-alpha-induced lipolysis in 3T3-L1 adipocytes via activating sirtuin 1 pathways

2021 ◽  
Author(s):  
Yu-Hong Yang ◽  
Yi-Ming Hao ◽  
Xiaofang Liu ◽  
Xiang Gao ◽  
Baozhen Wang ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Docosahexaenoic Acid ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Sirtuin 1 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Inhibit Tumor Necrosis Factor

Some chronic diseases such as cancer-associated cachexia (CAC) and obesity are associated with overproduction of tumor necrosis factor-alpha (TNF-α), which stimulates excess lipolysis in adipocytes. Our previous studies manifested that...

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