scholarly journals Granuloma Necrosis during Mycobacterium avium Infection Does Not Require Tumor Necrosis Factor

2004 ◽  
Vol 72 (10) ◽  
pp. 6139-6141 ◽  
Author(s):  
Manuela Flórido ◽  
Rui Appelberg
Keyword(s):  
Tumor Necrosis Factor ◽  
Mycobacterium Avium ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Low Doses ◽  
Avium Infection ◽  
Interferon Responses ◽  
Mycobacterium Avium Infection ◽  
Deficient Mice ◽  
Necrosis Factor

ABSTRACT The infection of tumor necrosis factor (TNF)-deficient mice with low doses of the virulent Mycobacterium avium strain 25291 led to the appearance of necrotic granulomas at 93 days of infection, i.e., sooner than necrotic granulomas appeared in C57BL/6 animals. Additionally, TNF-deficient mice exhibited higher mycobacterial loads in the infected organs, had extremely exacerbated gamma interferon responses as evaluated in the sera of infected animals, and showed reduced survival. Thus, TNF is not required for granuloma necrosis.

Ethanol modulation of tumor necrosis factor and gamma interferon production by murine splenocytes and macrophages

Life Sciences ◽  
1993 ◽  
Vol 52 (15) ◽  
pp. 1319-1326 ◽  
Author(s):  
Guan-jie Chen ◽  
Dennis S. Huang ◽  
Bernhard Watzl ◽  
Ronald R. Watson
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Interferon Production ◽  
Murine Splenocytes ◽  
Necrosis Factor

Immunodeficiency of Tumor Necrosis Factor and Lymphotoxin-α Double-Deficient Mice

1998 ◽  
pp. 103-118 ◽  
Author(s):  
Hans-Pietro Eugster ◽  
Matthias Müller ◽  
Michel Le Hir ◽  
Bernhard Ryffel
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Lymphotoxin Α ◽  
Deficient Mice ◽  
Necrosis Factor

scholarly journals Gamma Interferon and Lipopolysaccharide Interact at the Level of Transcription To Induce Tumor Necrosis Factor Alpha Expression

2001 ◽  
Vol 69 (5) ◽  
pp. 2847-2852 ◽  
Author(s):  
Julia Y. Lee ◽  
Kathleen E. Sullivan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Gamma Interferon ◽  
Necrosis Factor Alpha ◽  
Rnase Protection ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT Lipopolysaccharide (LPS) is a very potent inducer of tumor necrosis factor alpha (TNF-α) expression from monocytes and macrophages. Another inflammatory cytokine, gamma interferon (IFN-γ), can potentiate the effects of LPS, but the mechanism is not thoroughly understood. Previous reports emphasized the ability of IFN-γ to upregulate CD14 expression (the receptor for LPS), and nearly all studies have utilized sequential stimulation with IFN-γ followed by LPS to exploit this phenomenon. This study demonstrates that IFN-γ can upregulate the effect of LPS at the level of transcription. Human monoblastic Mono-Mac-6 cells produced up to threefold-greater levels of TNF-α when simultaneously stimulated with LPS and IFN-γ compared to treatment with LPS alone. RNase protection studies showed a similar increase in RNA beginning as early as within 30 min. The synthesis of TNF-α mRNA in IFN-γ- and LPS-treated Mono-Mac-6 cells was also temporally prolonged even though the message turnover rate was identical to that seen in LPS stimulated cells. The modulatory effect of IFN-γ may be mediated by Jak2.

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