To clarify the recovery patterns of spontaneous activity and liver damage after different stressors, female Fischer 344 rats were treated with Propionibacterium aches (P, aches) or water immersion stress before lipopolysaccharide (LPS) injection. They were then examined for wheel running activity, serum corticosterone concentration, serum alanine aminotransferase (ALT) activity, histological appearance of liver and plasma tumor necrosis factor alpha (TNF-a) concentration.
The recovery in physical activity of P. aches-treated rats was faster than that of water immersion rats. One day after the stressors, serum corticosterone cancentration and ALT activity of P. acnes-treated rats were higher than that of water immersion rats. In addition, increases in serum ALT activity and plasma TNF- a, as well as massive necrosis of the liver in P. acnes-treated rats were observed seven days after stress treatment. The P. acnes-LPS rats also showed a reduction in survival rate after 24 hours. These results suggest that P. acnes stress causes serious inflammation when stimulated by LPS. Although rapid recovery in physical activity was not inhibited by P. acnes stress, it differed from the response of water immersion stress.

To determine whether lipopolysaccharide (LPS)-induced prostaglandin (PG) E2 production is responsible for reduced spontaneous physical activity, we measured LPS ( 1 mg/kg, i. v.)-induced changes in voluntary wheel-running activity for 24 hours in both C3H/HeJ (LPS unresponsive due to a mutation in the tlr4 gene) and C3H/HeN (LPS response) mice. We also examined the effect of tlr4-gene mutation on LPS-induced PGE2 production using peritoneal macrophages from the C3H/HeJ and C3H/HeN mice. In addition, the voluntary wheel-running activity of the C3H/HeN mice, which were injected with the PGE2 inhibitor indomethacin (IM ; 0-20 mg/kg, i. p.) 30 min before injection with or without LPS ( 1 mg/kg), was monitored for 24 hours. Wheel-running activity in the C3H/HeJ mice was maintained in spite of LPS injection, but the activity in the C3H/HeN mice was significantly reduced by LPS injection. In vitro experiment showed peritoneal macrophage PGE2 production to be lower in the C3H/HeJ mice than that in the C3H/HeN mice. IM partially, but significantly, attenuated the LPS-induced reduction in wheel-running activity in the C3H/HeN mice. Our results suggest that the transient reduction in physical activity after LPS injection is partially mediated by LPS-induced PGE2 production, and that other factors also play a role.

To clarify the recovery patterns of spontaneous activity and liver damage after different stressors, female Fischer 344 rats were treated with Propionibacterium aches (P, aches) or water immersion stress before lipopolysaccharide (LPS) injection. They were then examined for wheel running activity, serum corticosterone concentration, serum alanine aminotransferase (ALT) activity, histological appearance of liver and plasma tumor necrosis factor alpha (TNF-a) concentration.
The recovery in physical activity of P. aches-treated rats was faster than that of water immersion rats. One day after the stressors, serum corticosterone cancentration and ALT activity of P. acnes-treated rats were higher than that of water immersion rats. In addition, increases in serum ALT activity and plasma TNF- a, as well as massive necrosis of the liver in P. acnes-treated rats were observed seven days after stress treatment. The P. acnes-LPS rats also showed a reduction in survival rate after 24 hours. These results suggest that P. acnes stress causes serious inflammation when stimulated by LPS. Although rapid recovery in physical activity was not inhibited by P. acnes stress, it differed from the response of water immersion stress.