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Decreased nitric oxide-mediated natural killer cell activation in Chronic Fatigue Syndrome (CFS)

  [ 108 votes ]   [ Discuss This Article ]
By Ogawa M, Nishiura T, Yoshimura M, Horikawa Y, Yoshida H, Okajima Y, Matsumura I, Ishikawa J, Nakao H, Tomiyama Y, Kanayama Y, Kanakura Y, Matsuzawa Y • • November 13, 1998

BACKGROUND: L-Arginine (L-Arg), one of the essential amino
acids, has been reported to have an immunomodulatory effect.
The precise mechanism of the L-Arg-induced natural killer (NK)
cell activation remains unresolved,and the effect of L-Arg on
NK cells in chronic fatigue syndrome (CFS) patients has not
been estimated.

METHODS: NK cell function was evaluated in 20
subjects with CFS and compared with that in 21 healthy

RESULTS: In healthy control subjects, NK activity
was significantly increased after treatment with L-Arg, an NK
function enhancer, for 24 h, whereas the same treatment failed
to enhance NK activity in the CFS patients. We thus focused on
L-Arg metabolism, which involves nitric oxide (NO) production
through NO synthase (NOS). The expression of inducible NO
synthase (iNOS) transcripts in peripheral blood mononuclear
cells was not significantly different between healthy control
subjects and CFS patients. The L-Arg- mediated NK cell
activation was abolished by addition of NG-monomethyl-
L-arginine, an inhibitor for iNOS. Furthermore, incubation
with S- nitroso-N-acetyl-penicillamine, an NO donor,
stimulated NK activity in healthy control subjects but not in
CFS patients.

CONCLUSION: These results demonstrate that the
L-Arg-induced activation of NK activity is mediated by NO and
that a possible dysfunction exists in the NO- mediated NK cell
activation in CFS patients.

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