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1 Department of Pediatrics, Section of Leukocyte Biology, Baylor College of Medicine, Houston, Texas, USA
2 Department of Pediatrics, Section of Leukocyte Biology, Baylor College of Medicine, Houston, Texas, USA; Department of Pediatrics/Critical Care, Baylor College of Medicine, Houston, Texas, USA
3 Department of Pediatrics, Section of Leukocyte Biology, Baylor College of Medicine, Houston, Texas, USA; ARS Childrens Nutrition Research Center, USDA, Houston, Texas, USA
* To whom correspondence should be addressed. E-mail: Chantalr{at}bcm.tmc.edu.
Hindlimb unloading (HU) is known to induce physiological alterations in various organ systems that mimic some responses observed following exposure to microgravity. In the present study, the effects of up to 4 weeks of HU on the liver were assessed in male Wistar rats and two mouse strains: endotoxin-sensitive C57BL/6 mice and endotoxin-resistant C3H/HEJ mice. Plasma levels of endotoxin, a known stimulator of hepatic injury, were measured in portal and systemic blood samples. Endotoxin was elevated by approximately 50% in portal blood samples of mice and rats, but was not detectable in systemic blood. This low-grade portal endotoxemia was associated with hepatic injury in rats and C57BL/6 mice as indicated by inflammation and elevated serum transaminase activities. Blood levels of the cytokine TNF-
were increased by approximately 50% in C57BL/6 mice; no significant elevation of this cytokine was detected in rats. Messenger RNA levels of the acute phase proteins serum amyloid A, haptoglobin and lipopolysaccharide binding protein were significantly enhanced after 3 weeks of HU in endotoxin-sensitive rodents. In contrast, no histological changes or significant increases in serum enzyme activity were detected following HU in C3H/HEJ mice despite portal endotoxin levels of 222 ± 83.4 pg/ml. At the 3-week time point, expression of acute phase proteins was not elevated in C3H/HEJ mice; however expression after 4 weeks of HU was similar to endotoxin-sensitive rodents. In conclusion, these findings indicate that HU induced portal endotoxemia, which likely contributed to the observed hepatic injury in endotoxin-sensitive rodents.
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