Sunday, October 9, 2011

RES: Evidence for inflammation and activation of cel l-mediated immunity in Myalgic Encephalomyelitis/Chronic Fat igue Syndrome (ME/CFS): Increased interleukin-1, tumor necro sis factor-=?ISO-8859-7?Q?=E1,?= PMN-elastase, lysozyme and neopterin

Note: Most humans respond to infection with inflammation. Viral
infection is associated with a vigorous inflammatory response
characterized by cellular infiltration and release of the
proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis
factor alpha (TNF-). In fact acute viral infection studies find that
initial infection severity is the single best predictor of persistent
fatigue.

In Klimas et al 2007 the authors discuss these variables: " ...A
number of symptoms of CFS are linked to inflammatory processes (eg,
lymphadenopathy, sore throat, myalgia, arthralgia), which has led many
researchers to hypothesize that immune dysfunction causes the illness.
CFS has been found to be associated with increased immune activation
and inflammatory cytokine levels, with subgroups demonstrating viral
reactivation and decreased cytotoxicity, alterations in lymphocyte
function, activation, and subset distributions. In addition, our
expanded understanding of the genomics of CFS has reinforced the
evidence that the illness is rooted in a biologic pathogenesis that
involves cellular dysfunction and interactions between the physiologic
stress response and inflammation..."


J Affect Disord.=A02011 Oct 3. [Epub ahead of print]

Evidence for inflammation and activation of cell-mediated immunity in
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Increased
interleukin-1, tumor necrosis factor-=E1, PMN-elastase, lysozyme and
neopterin.

Maes M,=A0Twisk FN,=A0Kubera M,=A0Ringel K.
Maes Clinics @ TRIA, Bangkok, Thailand.

Abstract

BACKGROUND:

There is evidence that inflammatory pathways and cell-mediated
immunity (CMI) play an important role in the pathophysiology of
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

Activation of inflammatory and CMI pathways, including increased
levels of cytokines, is known to induce fatigue and somatic symptoms.

Given the broad spectrum inflammatory state in ME/CFS, the aim of this
study was to examine whether inflammatory and CMI biomarkers are
increased in individuals with ME/CFS.

METHODS:

In this study we therefore measured plasma interleukin-(IL)1, tumor
necrosis factor (TNF)=E1, and PMN-elastase, and serum neopterin and
lysozyme in 107 patients with ME/CFS, 37 patients with chronic fatigue
(CF), and 20 normal controls. The severity of ME/CFS was measured with
the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale.

RESULTS:

Serum IL-1, TNF=E1, neopterin and lysozyme are significantly higher in
patients with ME/CFS than in controls and CF patients.

Plasma PMN-elastase is significantly higher in patients with ME/CFS
than in controls and CF patients and higher in the latter than in
controls.

Increased IL-1 and TNF=E1 are significantly correlated with fatigue,
sadness, autonomic symptoms, and a flu-like malaise; neopterin is
correlated with fatigue, autonomic symptoms, and a flu-like malaise;
and increased PMN-elastase is correlated with concentration
difficulties, failing memory and a subjective experience of infection.

CONCLUSIONS:

The findings show that ME/CFS is characterized by low-grade
inflammation and activation of CMI. The results suggest that
characteristic symptoms of ME/CFS, such as fatigue, autonomic symptoms
and a flu-like malaise, may be caused by inflammatory mediators, e.g.
IL-1 and TNF=E1.

Copyright =A9 2011 Elsevier B.V. All rights reserved.

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