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Interleukin-1 beta, interleukin-1 receptor antagonist, & soluble interleukin-1 receptor type II secretion in Chronic Fatigue Syndrome (CFS)

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Chronic fatigue syndrome is a condition that affects women in
disproportionate numbers, and that is often exacerbated in the
premenstrual period and following physical exertion. The signs
and symptoms, which include fatigue, myalgia, and low-grade
fever, are similar to those experienced by patients infused
with cytokines such as interleukin-1.

The present study was carried out to test the hypotheses that (1)
cellular secretion of interleukin-1 beta (IL-1 beta), interleukin-1
receptor antagonist (IL-1Ra), and soluble interleukin-1 receptor
type II (IL-1sRII) is abnormal in female CFS patients compared
to age- and activity-matched controls; (2) that these
abnormalities may be evident only at certain times in the
menstrual cycle; and (3) that physical exertion (stepping up
and down on a platform for 15 min) may accentuate differences
between these groups.

Isolated peripheral blood mononuclear cells from healthy #
women, but not CFS patients, exhibited significant
menstrual cycle-related differences in IL-1 beta
secretion that were related to estradiol and progesterone
levels (R2 = 0.65, P < 0.01). IL-1Ra secretion for CFS
patients was twofold higher than controls during the
follicular phase (P = 0.023), but luteal-phase levels were
similar between groups. In both phases of the menstrual cycle,
IL-1sRII release was significantly higher for CFS patients
compared to controls (P = 0.002). The only changes that might
be attributable to exertion occurred in the control subjects
during the follicular phase, who exhibited an increase in IL-1
beta secretion 48 hr after the stress (P = 0.020).

These results suggest that an abnormality exists in IL-1 beta
secretion in CFS patients that may be related to altered
sensitivity to estradiol and progesterone. Furthermore, the
increased release of IL-1Ra and sIL-1RII by cells from CFS
patients is consistent with the hypothesis that CFS is
associated with chronic, low-level activation of the immune
system.

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