scholarly journals Faculty Opinions recommendation of Gamma interferon, tumor necrosis factor alpha, and nitric oxide synthase 2, key elements of cellular immunity, perform critical protective functions during humoral defense against lethal pulmonary Yersinia pestis infection.

2006 ◽  
Author(s):  
James Bliska
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Cellular Immunity ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase ◽  
Necrosis Factor

Tumor necrosis factor-alpha alters pulmonary vasoreactivity via neutrophil-derived oxidants

1993 ◽  
Vol 265 (5) ◽  
pp. L462-L471 ◽  
Author(s):  
T. J. Ferro ◽  
D. C. Hocking ◽  
A. Johnson
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Vascular Effects ◽  
Lung Weight ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Reactive Oxidant ◽  
Necrosis Factor

We postulated that tumor necrosis factor-alpha (TNF) “primes” the lung for the development of pulmonary vasoconstriction and edema by inducing the release of polymorphonuclear leukocyte (PMN)-derived reactive oxidant species (ROS). Guinea pigs were injected with TNF (1.6 x 10(5) U/kg ip), and the lungs isolated 18 h later. Compared with controls, TNF pretreatment resulted in 1) greater increases in lung weight and capillary pressure in response to the thromboxane A2 mimetic U-46619 (365 pmol/min) and 2) an increase in the dose of acetylcholine (ACh) causing 50% of maximal dilation (EC50). The vascular effects of TNF were associated with 1) decreased lung effluent nitrite (NO2-, oxidation product of nitric oxide), 2) increased lung effluent superoxide (O2-), and 3) increased lung myeloperoxidase (MPO). Superoxide dismutase (SOD, 10 U/ml) prevented 1) the effects of TNF on the hemodynamic responses to U-46619 and ACh and 2) the TNF-induced decrease in NO2-. The effects of TNF on lung MPO and effluent O2- were prevented using cyclophosphamide intraperitoneally (100 mg/kg 5 days before, and 50 mg/kg 1 day before, treatment with TNF or control). The data suggest that ROS generated from PMN mediate the decrease in nitric oxide and altered pulmonary vasoreactivity induced by TNF.

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