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

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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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