Antiserum against tumor necrosis factor enhances lipopolysaccharide fever in rats

1990 ◽  
Vol 258 (2) ◽  
pp. R332-R337 ◽  
Author(s):  
N. C. Long ◽  
S. L. Kunkel ◽  
A. J. Vander ◽  
M. J. Kluger
Keyword(s):  
Tumor Necrosis Factor ◽  
Intramuscular Injection ◽  
Tumor Necrosis ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Control Serum ◽  
Necrosis Factor

The role of tumor necrosis factor (TNF, cachectin), a putative endogenous pyrogen, was investigated by comparing fever and plasma TNF levels after the intraperitoneal and intramuscular injection of 10 micrograms/kg lipopolysaccharide (LPS) into male Sprague-Dawley rats and by neutralization of endogenous TNF using TNF antiserum. An intraperitoneal injection of LPS caused a biphasic fever that lasted approximately 6.5 h. TNF levels in these rats peaked at 657 +/- 222 U/ml at 1 h then declined to virtually undetectable levels by the fourth hour. The intramuscularly injected animals showed a lower monophasic fever and low sustained TNF levels (40 +/- 10 U/ml at 1 h, 18 +/- 11 U/ml at 4 h). In a second study, an antiserum that had been shown to neutralize rat TNF was injected intraperitoneally 2 h before the intramuscular injection of 10 micrograms/kg LPS. Control rats were injected with normal rabbit serum before LPS. During the second hour after the injection of LPS, the animals that received the antiserum developed fevers that tended to be lower than those seen in the rats that were injected with control serum (0.33 +/- 0.06 vs. 0.58 +/- 0.1), although this difference was not significant. However, during the third through eighth hours after LPS, the antiserum-injected rats had mean body temperatures that were significantly higher than those of the control rats (1.62 +/- 0.11 vs. 1.07 +/- 0.09; P = 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

The role of the tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) in offspring exposed to prenatal hypoxia

2017 ◽  
Vol 9 (6) ◽  
pp. 661-669 ◽  
Author(s):  
L. M. Reyes ◽  
A. Shah ◽  
A. Quon ◽  
J. S. Morton ◽  
S. T. Davidge
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Female Offspring ◽  
Prenatal Hypoxia ◽  
Adult Offspring ◽  
Cardiomyocyte Proliferation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Oxygen Conditions ◽  
Necrosis Factor

Exposure to prenatal hypoxia in rats leads to intrauterine growth restriction (IUGR), decreases fetal cardiomyocyte proliferation and increases the risk to develop cardiovascular diseases (CVD) later in life. The tumor necrosis factor-related weak inducer of apoptosis (TWEAK) induces cardiomyocyte proliferation through activation of the fibroblast growth factor-inducible molecule 14 (Fn-14) receptor. The TWEAK/Fn-14 pathway becomes quiescent shortly after birth, however, it becomes upregulated with CVD; suggesting that it could be a link between the increased susceptibility to CVD in pregnancies complicated by hypoxia/IUGR. We hypothesized that offspring exposed to prenatal hypoxia will exhibit reduced cardiomyocyte proliferation due to reduced Fn-14 expression and that the TWEAK/Fn-14 pathway will be expressed in those adult offspring. We exposed pregnant Sprague Dawley rats to control (21% oxygen) or hypoxic (11% oxygen) conditions from gestational days 15 to 21. Ventricular cardiomyocytes were isolated from male and female, control and hypoxic offspring at postnatal day 1. Proliferation was assessed in the presence or absence of r-TWEAK (72 h, 100 ng/ml). Prenatal hypoxia was not associated with differences in Fn-14 protein expression in either male or female offspring. Cardiomyocytes from prenatal hypoxic male, but not female, offspring had decreased proliferation compared with controls. Addition of r-TWEAK increased cardiomyocyte proliferation in all offspring. In adult offspring of all groups, the TWEAK/Fn-14 pathway was not detectable. Cardiomyocyte proliferation was reduced in only male offspring exposed to prenatal hypoxia but this was not due to changes in the Fn-14 pathway. Studies addressing other pathways associated with CVD and prenatal hypoxia are needed.

Tumor necrosis factor is not involved in exercise-induced elevation in core temperature

1993 ◽  
Vol 265 (6) ◽  
pp. R1351-R1354 ◽  
Author(s):  
P. J. Rowsey ◽  
K. T. Borer ◽  
M. J. Kluger
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Control Serum ◽  
Exercise Induced ◽  
Running Wheels ◽  
Necrosis Factor

Female Sprague-Dawley rats (12:12-h light-dark photoperiod) with access to running wheels have an elevated body temperature (BT) both during exercise (nighttime) and nonexercise periods (daytime). We studied whether the exercise-induced increase in BT is modulated by the release of the cytokine, tumor necrosis factor-alpha (TNF). Two weeks after the onset of exercise, nighttime temperatures of exercising rats were elevated approximately 0.5 degree C compared with preexercise values (P = 0.006). By 3 wk after the onset of exercise, daytime temperatures had increased 0.3 degree C (P = 0.03) above control levels. To confirm that endogenously produced TNF can modulate fever in female rats, we injected six rats with antiserum to TNF (300 microliters/rat) and six rats with control serum 24 h before intraperitoneal injection of lipopolysaccharide (50 micrograms/kg). As occurred in earlier studies on male rats, antiserum-treated female rats had significantly enhanced fevers (P = 0.017). To determine whether endogenously produced TNF was involved in modulating the daytime and nighttime increases in BT, antiserum to TNF (300 microliters/rat, n = 7) or control serum (300 microliters/rat, n = 5) was injected intraperitoneally in exercising rats. Neither injection of antiserum nor control serum had any effect on daytime or nighttime BTs. Because BTs of exercising female rats injected with antiserum against TNF were not affected, we conclude that TNF is not responsible for modulating their exercise-induced rise in BT.

Tumor necrosis factor-α induces vascular hyporesposiveness in sprague-dawley rats

Life Sciences ◽  
1992 ◽  
Vol 50 (19) ◽  
pp. 1437-1444 ◽  
Author(s):  
Katsutoshi Takahashi ◽  
Katsuyuki Ando ◽  
Ayumu Ono ◽  
Tatsuo Shimosawa ◽  
Etsuro Ogata ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Factor Α ◽  
Necrosis Factor
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