scholarly journals Inhibiting tumor necrosis factor‐alpha at time of induced intervertebral disc injury limits long‐term pain and degeneration in a rat model

JOR Spine ◽  
2018 ◽  
Vol 1 (2) ◽  
pp. e1014 ◽  
Author(s):  
Thomas W. Evashwick‐Rogler ◽  
Alon Lai ◽  
Hironobu Watanabe ◽  
Jonathan M. Salandra ◽  
Beth A. Winkelstein ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Intervertebral Disc ◽  
Tumor Necrosis Factor Alpha ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Disc Injury ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Induced myelopathy after long-term anti-tumor necrosis factor alpha treatment

2011 ◽  
Vol 9 (S1) ◽  
Author(s):  
C Modesto ◽  
F Caracsegui ◽  
S Melendo ◽  
A Sanchez-Montanez ◽  
Manel Roig
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Yersinia pestis YopJ Suppresses Tumor Necrosis Factor Alpha Induction and Contributes to Apoptosis of Immune Cells in the Lymph Node but Is Not Required for Virulence in a Rat Model of Bubonic Plague

2006 ◽  
Vol 74 (9) ◽  
pp. 5126-5131 ◽  
Author(s):  
Nadine Lemaître ◽  
Florent Sebbane ◽  
Daniel Long ◽  
B. Joseph Hinnebusch
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Rat Model ◽  
Immune Cells ◽  
Tumor Necrosis ◽  
Bubonic Plague ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT The virulence of the pathogenic Yersinia species depends on a plasmid-encoded type III secretion system that transfers six Yop effector proteins into host cells. One of these proteins, YopJ, has been shown to disrupt host cell signaling pathways involved in proinflammatory cytokine production and to induce macrophage apoptosis in vitro. YopJ-dependent apoptosis in mesenteric lymph nodes has also been demonstrated in a mouse model of Yersinia pseudotuberculosis infection. These results suggest that YopJ attenuates the host innate and adaptive immune response during infection, but the role of YopJ during bubonic plague has not been completely established. We evaluated the role of Yersinia pestis YopJ in a rat model of bubonic plague following intradermal infection with a fully virulent Y. pestis strain and an isogenic yopJ mutant. Deletion of yopJ resulted in a twofold decrease in the number of apoptotic immune cells in the bubo and a threefold increase in serum tumor necrosis factor alpha levels but did not result in decreased virulence, systemic spread, or colonization levels in the spleen and blood. Our results indicate that YopJ is not essential for bubonic plague pathogenesis, even after peripheral inoculation of low doses of Y. pestis. Instead, the effects of YopJ appear to overlap and augment the immunomodulatory effects of other Y. pestis virulence factors.

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