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Cytokine dysregulation in the post-Q-fever fatigue syndrome

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By Penttila IA, Harris RJ, Storm P, Haynes D, Worswick DA, Marmion BP • www.ProHealth.com • August 26, 1998


The post-Q-fever fatigue syndrome (QFS) (inappropriate fatigue,
myalgia and arthralgia, night sweats, changes in mood and
sleep patterns) follows about 20% of laboratory-proven, acute
primary Q-fever cases. Cytokine dysregulation resulting from
chronic immune stimulation and modulation by persistence of
Coxiella burnetii cells or their antigens is hypothesized. We
studied cytokine release patterns of peripheral blood
mononuclear cells (PBMC) stimulated with various ligands in
short- term culture, from 18 patients with active QFS, and 27
controls: six with resolving QFS, five who had had acute
primary Q-fever without subsequent QFS, eight healthy Q-fever
vaccinees and eight healthy subjects without Q-fever antibody.
Conditioned media (CM) from PBMC stimulated in short-term
culture with Q-fever antigens, PHA or measles antigen (as an
unrelated antigen) were assayed for IL-2, IL-4, IL-5, IL- 6,
IL-10 and IFN gamma by AgEIA, and for IL-1 and TNF alpha/beta
by bioassay. Aberrant cytokine release patterns were observed
with PBMC from QFS patients when stimulated with Q-fever
antigens: an accentuated release of IL-6 which was
significantly [p = 0.01, non-parametric one- way analysis of
variance (ANOVA)] in excess of medians for all four control
groups. With IL-2, the number of responders in the active QFS
group was decreased relative to control groups (Fisher's exact
test, p = 0.01) whereas the number of IFN gamma responders was
increased (Fisher's exact test, p = 0.0008). Significant
correlations were observed between concentrations of IL-6 in
CM, total symptom scores, and scores for other key symptoms.




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