INTERFERON-?? AND BACTERIAL LIPOPOLYSACCHARIDE ACT SYNERGISTICALLY ON HUMAN NEUTROPHILS ENHANCING INTERLEUKIN-8, INTERLEUKIN-1??, TUMOR NECROSIS FACTOR-??, AND INTERLEUKIN-12 P70 SECRETION AND PHAGOCYTOSIS VIA UPREGULATION OF TOLL-LIKE RECEPTOR 4

Shock ◽  
2007 ◽  
Vol 27 (3) ◽  
pp. 226-231 ◽  
Author(s):  
Michal Pearl-Yafe ◽  
Ina Fabian ◽  
Drora Halperin ◽  
Edith Flatau ◽  
Sara Werber ◽  
...  
Author(s):  
Kouji Matsushima ◽  
Christian G. Larsen ◽  
Ajoy K. Samanta ◽  
Naofumi Mukaida ◽  
Arthur O. Anderson ◽  
...  

1992 ◽  
Vol 175 (4) ◽  
pp. 1123-1129 ◽  
Author(s):  
J R Lane ◽  
D A Neumann ◽  
A Lafond-Walker ◽  
A Herskowitz ◽  
N R Rose

We have previously demonstrated that bacterial lipopolysaccharide (LPS) is capable of promoting Coxsackie B3 (CB3)-induced myocarditis in genetically resistant B10.A mice. Because LPS is known to increase production of various cytokines, we tested CB3-infected, LPS-treated mice for the presence of interleukin 1 (IL-1) and tumor necrosis factor (TNF). We found significantly increased amounts of both cytokines in the sera of CB3/LPS-treated mice compared with animals treated only with LPS. We also found immunohistochemical evidence for local production of these cytokines in the cardiac tissue of CB3/LPS-treated mice. Treatment with IL-1 or TNF alone promoted CB3-induced autoimmune myocarditis in resistant B10.A mice. Myocarditis was also observed when uninfected mice were immunized with syngeneic heart extract in the presence of IL-1 or TNF.


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