Cytokines across the Night in Chronic Fatigue Syndrome with and without Fibromyalgia

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Cytokines across the Night in Chronic Fatigue Syndrome with and without Fibromyalgia

[sb: I couldn't find this posted anywhere. Broderick's latest is with Klimas' cohort I think]

Toru Nakamura,1,2 Stephan K. Schwander,3* Robert Donnelly,3 Felix Ortega,3 Fumiharu Togo,4 Gordon Broderick,5 Yoshiharu Yamamoto,6 Neil S. Cherniack,1,3,{dagger} David Rapoport,7 and Benjamin H. Natelson1,2*

Pain & Fatigue Study Center,1 Departments of Neurosciences,2 Medicine, UMDNJNew Jersey Medical School, Newark, New Jersey 07103,3 Department of Work Stress Control, Japan National Institute of Occupational Safety and Health, Kawasaki 214-8585, Japan,4 Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Canada,5 Educational Physiology Laboratory, Graduate School of Education, The University of Tokyo, Tokyo, Japan,6 Department of Medicine, Division of Pulmonary and Critical Care Medicine, NYU School of Medicine, New York, New York 100167

Received 22 September 2009/ Returned for modification 4 November 2009/ Accepted 12 February 2010

The symptoms of chronic fatigue syndrome (CFS) are consistent with cytokine dysregulation. This has led to the hypothesis of immune dysregulation as the cause of this illness. To further test this hypothesis, we did repeated blood sampling for cytokines while patients and matched healthy controls slept in the sleep lab. Because no one method for assaying cytokines is acknowledged to be better than another, we assayed for protein in serum, message in peripheral blood lymphocytes (PBLs), and function in resting and stimulated PBLs. We found no evidence of proinflammatory cytokine upregulation. Instead, in line with some of our earlier studies, we did find some evidence to support a role for an increase in interleukin-10, an anti-inflammatory cytokine. Although the changes were small, they may contribute to the common complaint in CFS patients of disrupted sleep.

Clinical and Vaccine Immunology, April 2010, p. 582-587, Vol. 17, No. 4
1071-412X/10/$12.00+0 doi:10.1128/CVI.00379-09
Copyright 2010, American Society for Microbiology. All Rights Reserved.
 

flybro

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Instead, in line with some of our earlier studies, we did find some evidence to support a role for an increase in interleukin-10, an anti-inflammatory cytokine. Although the changes were small, they may contribute to the common complaint in CFS patients of disrupted sleep.
Could anyone hazzard a guess as to wether this increase in interluken-10 could have any links to night sweats?
 
G

Gerwyn

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Could anyone hazzard a guess as to wether this increase in interluken-10 could have any links to night sweats?
This might help

Interleukin-10 (cytokine synthesis inhibitory factor) acts in the central nervous system of rats to reduce sleep.

OPP MR, SMITH EM, HUGHES TK JR.
J Neuroimmunol 1995;60(1-2):165-8
Department of Psychiatry and Behavioral Sciences, University of Texas Medical Branch, Galveston, TX 77555-0428, USA

Abstract:


Interleukin-10 (IL-10), originally designated a cytokine synthesis inhibitory factor, inhibits the synthesis of the pro-inflammatory cytokines IL-1 and tumor necrosis factor by stimulated human and mouse monocytes/macrophages; these cytokines are involved in the regulation of sleep. To determine if IL-10 reduces spontaneous sleep, we injected murine recombinant IL-10 intracerebroventricularly into rats prior to light onset. Non-rapid eye movements sleep was reduced. The behavioral responses to IL-10 were abolished by heat-inactivation of this cytokine. We believe these to be the first observations of central nervous system actions for this cytokine. These results further support the hypothesis that cytokines are involved in the regulation of sleep, and suggest an additional mechanism whereby sleep may be altered in response to an activated immune system.
 

flybro

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Cheers Gerwyn,

I dont fully understand it, but I get the feeling it hodls up my statement to the Docs that I am convinced the night sweats are linked to an underlying infection, and that the only thing that has helped this has been clarythromycin, which reduces the night sweats dramatically.

It also seems to reduce pelvic inflamation pain as well.
Another thing is that when i start a round of clarithromycin I am dog tired and sleep like a baby, for 2 or three days, by which time my overall health improves.
 

ramakentesh

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Arent interluekins the messenger between the immune system and the automomic nervous system? isnt CFS associated with chronic inflammation? Id wager this small variation was just the result of other mechanisms such as overall sympathetic excess.
Post exertional malaise in POTS and muscular dystrophy is associated with reduced neuronal nitric oxide - through increased oxidisive stress. Id also wager its the same in CFS
 

Dolphin

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Some info from the full paper

Here's info from the intro:

However, a very different and alternative hypothesis focuses
on the common complaint in CFS of unrefreshing sleep (4).
Recent work suggests that sleep is under the control of a
cytokine/sleep network where normal sleep follows a balanced
secretion of pro- and anti-inflammatory cytokines (13). We
hypothesized that CFS might result from an imbalance of this
network in favor of the anti-inflammatory cytokines which are
sleep disrupting (14). Supporting this possibility is the result of
a recent study (28) in which we sampled blood for cytokines
every 20 min across a 24-h day in patients with fibromyalgia
(FM) (28), a medically unexplained, diffuse pain syndrome that
has substantial overlap with CFS (5). Of several pro- and
anti-inflammatory cytokines studied, the only one to show differences
from controls, i.e., increases, was the anti-inflammatory
cytokine interleukin-10 (IL-10), and that was true only for
nocturnal data. Because no information was provided as to
whether this patient group also fulfilled criteria for CFS, it is
not appropriate to extend the results of that study to patients
with CFS. Thus, one purpose of the current study was to
determine if the results we obtained in patients with FM could
be extended to those with CFS. Moreover, because we hypothesized
disturbances in the cytokine/sleep network, we decided
to study cytokines during sleep with the expectation of finding
maximum differences at this time.

14. Kushikata, T., J. Fang, and J. M. Krueger. 1999. Interleukin-10 inhibits
spontaneous sleep in rabbits. J. Interferon Cytokine Res. 19:10251030.
Given this, I wonder would they find more in a group whose sleep pattern was off, either on that night or overall.

I know a lot of people with ME/CFS who do not sleep like this either regularly, or on "bad" nights:

Patients were then allowed to go to sleep between 10:30 and
11:00 p.m. while being monitored. Three additional blood samples were taken at
approximately 1:00 a.m., 3:00 a.m., and 5:00 a.m. Subjects then awoke between
7:00 and 7:30 a.m., after which a final blood sample was taken.
There were a few findings:
The expression level of IL-10 for the CFS without FM subgroup was significantly
higher than that of healthy control subjects or the group
with CFS and FM. In addition, CFS patients with FM tended
to have decreased IL-1b (P = 0.068) compared with control
subjects.

Exploration for correlations between cytokine data and clinical
variables was negative except for a tendency toward lower
IL-8 values with higher CFS severity score (r = 20.44; P =
0.058). Scores for patients with CFS alone did not differ in
severity from those with CFS plus FM (Table 1). There was a
significant correlation between total sleep period and IL-10
(r = -0.33; P < 0.042) in patients.

The mixed model analysis reiterated our group analysis by
showing a significant difference in only IL-10 levels. Figure 1
shows the distribution of IL-10 data over time. CFS patients
without FM showed higher IL-10 values than controls at 3:00
and 5:00 a.m. and higher values than for subjects with CFS and
FM at 5:00 a.m.
ELISPOT assay: group differences in cytokines under basal
conditions.

[..]
As had been the case with plasma protein, IL-1b
tended to be lower in CFS subjects than controls (P = 0.099).
qRT-PCR assay.

[..]

IL-1b showed a tendency toward increased levels in
patients with higher severity scores (r = 0.34; P = 0.094);
however, we found no significant correlation between IL-1b
and CFS severity in the PCR assay.

-----
the modest change in
IL-10 reported here is consistent with the suggestion that patients
with CFS show a shift toward Th2-type cytokines.