Volgens een studie van onderzoekers van de NCNED van de Griffith University (Australië) van
6 ME/CVS-patiënten (diagnose op basis van de Canadese Criteria) en 6 gezonde 'proefkonijnen'
is de werking van een specifiek ionen-kanaal (TRPM3) in ME/CVS sterk verminderd.
Dit ionen-kanaal draagt er toe bij dat de cel, indien nodig, calcium kan opnemen.
Intracellulair calcium is essentieel voor uiteenlopende (basis)functies van een cel.
NK-cellen hebben calcium nodig om goed te kunnen functioneren en zieke cellen uit te schakelen.
Een studie uit 2017 toonde
aan dat het aantal TRPM3-kanalen (na stimulatie) ook verminderd is.
Het betreft hier een kleine studie en het onderzoek werd uitgevoerd op NK-cellen.
Echter als de bevindingen op grotere schaal in andersoortige cellen bevestigd worden,
heeft dit grote implicaties voor patiënten (symptoombehandeling) en beleidsmakers (CGT/GET).
Senator Steele-John stelt naar aanleiding van dit onderzoek in de media:
"For me, the biggest take away from this breakthrough is
that it is neither a physiological or a psychological condition; it is pathological.
Graded exercise therapy and cognitive behavioural therapy
simply do not, and cannot work, for people suffering with ME/CFS,"
Senator Steele-John said.
"Forcing someone to do exercise
when their muscle cells are not producing enough ions to work properly
is nothing short of cruelty, and
these kind of treatment programs must end
so that proper treatments can be found."
Voor de volledige tekst van het artikel, klik op onderstaande afbeelding:
Loss of Transient Receptor Potential Melastatin 3 ion channel function in natural killer cells
from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.
Mol Med. 2018 Aug 14;24(1):44. doi: 10.1186/s10020-018-0046-1.
Cabanas H, Muraki K, Eaton N, Balinas C, Staines D, Marshall-Gradisnik S.
Abstract
BACKGROUND:
Chronic Fatigue Syndrome (CFS)/Myalgic Encephalomyelitis (ME) is a debilitating disorder
that is accompanied by reduced cytotoxic activity in natural killer (NK) cells.
NK cells are an essential innate immune cell,
responsible for recognising and inducing apoptosis of tumour and virus infected cells.
Calcium is an essential component in mediating this cellular function.
Transient Receptor Potential Melastatin 3 (TRPM3) cation channels
have an important regulatory role in mediating calcium influx to help maintain cellular homeostasis.
Several single nucleotide polymorphisms have been reported in TRPM3 genes
from isolated peripheral blood mononuclear cells, NK and B cells in patients with CFS/ME and
have been proposed to correlate with illness presentation.
Moreover, a significant reduction in
both TRPM3 surface expression and intracellular calcium mobilisation in NK cells
has been found in CFS/ME patients compared with healthy controls.
Despite the functional importance of TRPM3,
little is known about the ion channel function in NK cells and the epiphenomenon of CFS/ME.
The objective of the present study was
to characterise the TRPM3 ion channel function in NK cells from CFS/ME patients
in comparison with healthy controls using whole cell patch-clamp techniques.
METHODS:
NK cells were isolated from 12 age- and sex-matched healthy controls and CFS patients.
Whole cell electrophysiology recording has been used to assess TRPM3 ion channel activity
after modulation with pregnenolone sulfate and ononetin.
RESULTS:
We report a significant reduction in amplitude of TRPM3 current
after pregnenolone sulfate stimulation
in isolated NK cells from CFS/ME patients compared with healthy controls.
In addition, we found pregnenolone sulfate-evoked ionic currents through TRPM3 channels
were significantly modulated by ononetin in isolated NK cells from healthy controls
compared with CFS/ME patients.
CONCLUSIONS:
TRPM3 activity is impaired in CFS/ME patients
suggesting changes in intracellular Ca2+ concentration, which may impact NK cellular functions.
This investigation further helps to understand the intracellular-mediated roles in NK cells and
confirm the potential role of TRPM3 ion channels in the aetiology and pathomechanism of CFS/ME.
KEYWORDS:
Calcium; Chronic fatigue syndrome/Myalgic encephalomyelitis; Flow cytometry; Natural killer cells; Patch-clamp; Transient receptor potential Melastatin 3
PMID: 30134818
PMCID: PMC6092868
DOI: 10.1186/s10020-018-0046-1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092868/pdf/10020_2018_Article_46.pdf
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