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Cytokine dysregulation in the post-Q-fever fatigue syndrome

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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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1 Star2 Stars3 Stars4 Stars5 Stars (61) votes, average: 2.85 out of 5