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Susceptibility to immunologically mediated fatigue in C57BL/6 versus Balb/c mice

  [ 43 votes ]   [ Discuss This Article ] • November 5, 1996

Proinflammatory cytokines such as interleukin (IL)-1 and tumor
necrosis factor (TNF)-alpha have been proposed to play a role
in the pathogenesis of fatigue. In the present study we
compared the susceptibility of two mouse strains to
immunologically induced fatigue. Daily running of two strains
of mice, Balb/c and C57BL/ 6, was assessed after a single
injection of Corynebacterium parvum antigen (2 mg/mouse).
Spontaneous running activity of each animal was compared to
mean running distance prior to injection. To evaluate the
involvement of cytokines in fatigue development, C57BL/6 mice
were treated with antibodies to specific cytokines at the
time of challenge with C. parvum antigen. Also, cytokine mRNA
expression was analyzed in the brains of mice at different
time periods after immunologic challenge.

A significant
difference in running activity between the two mice strains
was observed after C. parvum antigen inoculation: C57BL/6
mice showing a greater (P < 0.05) reduction in running
activity (relative to preinjection levels) and slower
recovery to baseline than Balb/c mice. Injection of
antibodies specific to either IL-1beta or TNF-alpha did not
alter immunologically induced fatigue, suggesting a lack of
involvement of these cytokines produced outside of the
central nervous system (CNS). However, increased TNF-alpha
and IL-1beta mRNA expression was found in the brains of
C57BL/6 compared to that seen in Balb/c mice at 6, 10, and 15
days after C. parvum antigen injection. The elevated CNS
cytokine mRNA expression corresponded to development of
fatigue. These findings are consistent with the hypothesis
that expression of proinflammatory cytokines within the CNS
plays a role in the pathogenesis of immunologically mediated

Sheng WS, Hu S, Lamkin A, Peterson PK, Chao CC

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