Volgens twee recente studies van Maes en anderen:
Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome.
J Affect Disord. 2011 Oct 1. doi:10.1016/j.jad.2011.09.010.
Maes M, Twisk FNM, Kubera M, Ringel K, Leunis J, Geffard M.
Background
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is accompanied by
systemic IgA/IgM
responses against the lipopolysaccharides (LPS) of commensal bacteria;
inflammation, e.g. increased plasma interleukin-(IL)1 and tumor necrosis factor (TNF)α; and
activation of cell-mediated immunity (CMI), as demonstrated by increased neopterin.
Methods
To study the relationships
between the IgA/IgM responses to the LPS of microbiota,
inflammation, CMI and the symptoms of ME/CFS
we measured
the IgA/IgM responses to the LPS of 6 different enterobacteria,
serum IL-1, TNFα,
neopterin, and elastase
in 128 patients with ME/CFS and chronic fatigue (CF).
Severity of symptoms was assessed by
the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale.
Results
Serum IL-1, TNFα, neopterin and elastase
are significantly higher in patients with ME/CFS than in CF patients.
There are significant and positive associations
between the IgA responses to LPS and serum IL-1, TNFα, neopterin and elastase.
Patients with an abnormally high IgA response
show increased serum IL-1, TNFα and neopterin levels, and
higher ratings on irritable bowel syndrome (IBS)
than subjects with a normal IgA response.
Serum IL-1, TNFα and neopterin are significantly related to
fatigue, a flu-like malaise, autonomic symptoms, neurocognitive disorders, sadness and
irritability.
Conclusions
The findings show that
increased IgA responses to commensal bacteria in ME/CFS
are associated with inflammation and CMI activation,
which are associated with symptom severity.
It is concluded that
increased translocation of commensal bacteria
may be responsible for the disease activity
in some ME/CFS patients.
Keywords:
Chronic fatigue syndrome; inflammation; cytokines; depression; oxidative stress; leaky gut
http://www.sciencedirect.com/science/article/pii/S0165032711005362
Evidence for inflammation and activation of cell-mediated immunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS):
Increased interleukin-1, tumor necrosis factor-α, PMN-elastase, lysozyme and neopterin.
J Affect Disord. 2011. doi:10.1016/j.jad.2011.09.004.
Maes M, Twisk FNM, Kubera M, Ringel K.
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)α, 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, TNFα, 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 TNFα
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 TNFα.
http://www.sciencedirect.com/science/article/pii/S0165032711005301
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