Unravelling intracellular immune dysfunctions in CFS: interactions between protein kinase R, RNase L cleavage, elastase, 2008, Meeus et al

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Unravelling intracellular immune dysfunctions in chronic fatigue syndrome: interactions between protein kinase R activity, RNase L cleavage and elastase activity, and their clinical relevance
Mira Meeus 1, Jo Nijs, Neil McGregor, Romain Meeusen, Guy De Schutter, Steven Truijen, Marc Frémont, Elke Van Hoof, Kenny De Meirleir

https://pubmed.ncbi.nlm.nih.gov/18396793/
Open access

Abstract
This study examined possible interactions between immunological abnormalities and symptoms in CFS. Sixteen CFS patients filled in a battery of questionnaires, evaluating daily functioning, and underwent venous blood sampling, in order to analyse immunological abnormalities.

Ribonuclease (RNase) L cleavage was associated with RNase L activity (rs=0.570; p=0.021), protein kinase R (PKR) (rs=0.716; p=0.002) and elastase activity (rs=0.500; p=0.049).

RNase L activity was related to elastase (rs=0.547; p=0.028) and PKR activity (rs=0.625; p=0.010).

RNase L activity (rs=0.535; p=0.033), elastase activity (rs=0.585; p=0.017) and RNase L cleavage (rs=0.521; p=0.038) correlated with daily functioning.

This study suggests that in CFS patients an increase in elastase activity and subsequent RNase L cleavage is accompanied by increased activity of both the PKR and RNase L enzymes. RNase L and elastase activity are related to daily functioning, thus evidence supporting the clinical importance of these immune dysfunctions in CFS patients was provided.

 
They found elastase abnormalities in blood vessels in research done at Ninewells hospital, Dundee.

I seem to remember that another study said that they did not find but they selected patients carefully for the Dundee study - even when the research was published as fukuda it was the interpretation of fukuda that was closest to ME, if you see what I mean.

It was definitely important research that should have been taken further.
 
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