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Nyhetstips tisdag den 21 augusti 2007
Myalgisk
Encefalomyelit (ME), kroniskt trötthetssyndrom - ej inbillning utan finns i
cellerna
Tre nya forskningspublikationer
kring ME (även kallat kroniskt trötthetssyndrom) har publicerats i juli 2007
i Neuro Endocrinol Lett. med läkaren Michael Maes (Belgien) som en av författarna. Man har
bland annat funnit att transkriptionsfaktorn NFκβ (NF-kappa-beta,
nuclear factor kappa beta) är signifikant höjd hos ME-drabbade.
Transkriptionsfaktorn NFκβ har en central roll i att koordinera
genuttrycket hos en mängd gener som styr immun-responsen. Ökad NFκβ aktiverar systemet för inflammatorisk
respons och oxidativ stress. Forskningsfynden leder också till möjligheter
till att behandla ME-patienter med antioxidanter som inhiberar produktionen
av transkriptionsfaktorn NFκβ.
Titlarna till de tre vetenskapliga publikationerna är:
- "Decreased
expression of CD69 in chronic fatigue syndrome in relation to
inflammatory markers: evidence for a severe disorder in the early
activation of T lymphocytes and natural killer cells"
- "Not
in the mind but in the cell: increased production of cyclo-oxygenase-2
and inducible NO synthase in chronic fatigue syndrome." och
- "Not in the mind of neurasthenic lazybones but in the
cell nucleus: patients with chronic fatigue syndrome have increased production
of nuclear factor kappa beta"
Två av titlarna till publikationerna förklarar att ME är
en sjukdom som ej beror på inbillningssjuka hos patienterna, utan att det
finns biomedicinska avvikelser som förklarar deras symtom. Maes har visat att
vissa NFκβ inuti lymfocyter inte
bara är signifikant avvikande hos ME drabbade, utan även att de är
korrelerade till symtomens svårighetsgrad hos patienterna.
Nyhet saxad från Michael Maes
hemsida (http://www.michaelmaes.com/):
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July 2007: New
publication in press: Not in the mind but in the cell: increased production
of cyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.
Chronic fatigue syndrome (CFS) is a medically
unexplained disorder, characterized by profound fatigue, infectious,
rheumatological and neuropsychiatric symptoms. There is, however, some
evidence that CFS is accompanied by signs of increased oxidative stress and
inflammation in the peripheral blood. This paper examines the role of the
inducible enzymes cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS)
in the pathophysiology of CFS. Toward this end we examined the production
of COX-2 and iNOS by peripheral blood lymphocytes (PBMC) in 18 CFS patients
and 18 normal volunteers and examined the relationships between those
inflammatory markers and the severity of illness as measured by means of
the FibroFatigue scale and the production of the transcription factor
nuclear factor kappa beta (NFκβ).
We found that the production of COX-2 and iNOS was
significantly higher in CFS patients than in normal controls. There were
significant and positive intercorrelations between COX-2, iNOS and
NFκβ and between COX-2 and iNOS, on the one hand, and the
severity of illness, on the other. The production of COX-2 and iNOS by
PBMCs was significantly related to aches and pain, muscular tension,
fatigue, concentration difficulties, failing memory, sadness and a
subjective experience of infection.
The results suggest that
a) an intracellular inflammatory response in the white
blood cells plays an important role in the pathophysiology of CFS;
b) the inflammatory response in CFS is driven by the
transcription factor NFκβ;
c) symptoms, such as fatigue, pain, cognitive defects
and the subjective feeling of infection, indicates the presence of a
genuine inflammatory response in CFS patients; and
d) CFS patients may be treated with substances that
inhibit the production of COX-2 and iNOS.
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Michel Maes fynd kan också innebära
att man hittar en behandling för ME patienter. Texten nedan är saxat ur
publikationen "Not in the mind of neurasthenic lazybones but in
the cell nucleus: patients with chronic fatigue syndrome have increased
production of nuclear factor kappa beta":
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It is suggested that CFS patients should be treated with
antioxidants, which inhibit the production of NFkappabeta, such as
curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3
fatty acids.
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Curcumin är ett gul-orange färgämne
i gurkmeja och är en antioxidant. Quercitin/quercetin är en flavonid och
antioxidant med svagt gulaktig färg som förekommer i frukt, speciellt i
oskalade äpplen samt lök. Silimarin/silymarin kommer från Mariatistel (Silyum
Marianum) och är kraftig antioxidant som har visat sig ha en positiv inverkan
på leverceller. Silymarin är sammansatt av flera substanser som kallas
flavonoliganer, bl.a. silibinin. Lipoic Acid (ALA, Alpha Lipoic Acid) heter
liponsyra på svenska och är en kraftig antioxidant.
Längre ner på denna sida finns
abstract infogat från de tre aktuella vetenskapliga publikationerna. För alla
publikationer på http://pubmed.gov av Maes M
klicka här: Länk
till M Maes publikationer
/Kasper Ezelius ( http://me-cfs.se
)
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De
tre aktuella artiklarna av Michael Maes om ME (kroniskt trötthetssyndrom)
Decreased
expression of CD69 in chronic fatigue
syndrome in relation to inflammatory markers:
evidence for a severe disorder in the early
activation of T lymphocytes and natural killer cells.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Länk
till artikeln i PubMed
Journal: Neuro
Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead
of print]
Authors: Mihaylova I, Deruyter M, Rummens JL, Bosmans E,
Maes M.
Affiliation: MCare4U Outpatient Clinics, Belgium.
NLM Citation: PMID: 17693977
There is some evidence that patients with chronic fatigue
syndrome (CFS) suffer from immune abnormalities, such as
immune activation and decreased immune cell responsivity
upon polyclonal stimili. This study was designed to evaluate
lymphocyte activation in CFS by using a CD69 expression
assay. CD69 acts as a costimulatory molecule for T- and natural
killer (NK) cell activation.
We collected whole blood from CFS patients, who met CDC
criteria, and healthy volunteers. The blood samples were
stimulated with mitogens during 18 h and the levels of activated
T and NK cells expressing CD69 were measured on a Coulter
Epics flow cytometer using a three color immunofluorescence
staining protocol.
The expression of the CD69 activation marker on T cells (CD3+,
CD3+CD4+, and CD3+CD8+) and on NK cells (CD45+CD56+)
was significantly lower in CFS patients than in healthy subjects.
These differences were significant to the extent that a significant
diagnostic performance was obtained, i.e. the area under the
ROC curve was around 89%. No differences either in the
number of leukocytes or in the number or percentage of
lymphocytes, i.e. CD3, CD4, CD8 and CD19, could be found
between CFS patients and the controls. Patients with CFS show
defects in T- and NK cell activation.
Since induction of CD69 surface expression is dependent on
the activation of the protein kinase C (PKC) activation pathway,
it is suggested that in CFS there is a disorder in the early
activation of the immune system involving PKC.
``````````````````
Not in the mind
but in the cell: increased
production of cyclo-oxygenase-2 and inducible
NO synthase in chronic fatigue syndrome.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Länk
till artikeln i PubMed
Journal: Neuro
Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead
of print]
Authors: Maes M, Mihaylova I, Kubera M, Bosmans E.
Affiliation: MCare4U Outpatient Clinics, Belgium.
NLM Citation: PMID: 17693978
Chronic fatigue syndrome (CFS) is a medically unexplained
disorder, characterized by profound fatigue, infectious,
rheumatological and neuropsychiatric symptoms. There is,
however, some evidence that CFS is accompanied by signs of
increased oxidative stress and inflammation in the peripheral
blood. This paper examines the role of the inducible enzymes
cyclo-oxygenase (COX-2) and inducible NO synthase (iNOS) in
the pathophysiology of CFS.
Toward this end we examined the production of COX-2 and
iNOS by peripheral blood lymphocytes (PBMC) in 18 CFS
patients and 18 normal volunteers and examined the
relationships between those inflammatory markers and the
severity of illness as measured by means of the FibroFatigue
scale and the production of the transcription factor nuclear factor
kappa beta (NFkappabeta).
We found that the production of COX-2 and iNOS was
significantly higher in CFS patients than in normal controls.
There were significant and positive intercorrelations between
COX-2, iNOS and NFkappabeta and between COX-2 and
iNOS, on the one hand, and the severity of illness, on the other.
The production of COX-2 and iNOS by PBMCs was significantly
related to aches and pain, muscular tension, fatigue,
concentration difficulties, failing memory, sadness and a
subjective experience of infection.
The results suggest that
a) an intracellular inflammatory response in the white blood cells
plays an important role in the pathophysiology of CFS;
b) the inflammatory response in CFS is driven by the
transcription factor NFkappabeta;
c) symptoms, such as fatigue, pain, cognitive defects and the
subjective feeling of infection, indicates the presence of a
genuine inflammatory response in CFS patients; and
d) CFS patients may be treated with substances that inhibit the
production of COX-2 and iNOS.
``````````````````
Not in the mind of
neurasthenic lazybones
but in the cell nucleus: patients with chronic
fatigue syndrome have increased production of
nuclear factor kappa beta.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Länk
till artikeln i PubMed
Journal: Neuro
Endocrinol Lett. 2007 Jul 11;28(4) [Epub ahead
of print]
Authors: Maes M, Mihaylova I, Bosmans E.
Affiliation: MCare4U Outpatient Clinics, Belgium.
crc.mh@telenet.be.
NLM Citation: PMID: 17693979
There is now some evidence that chronic fatigue syndrome is
accompanied by an activation of the inflammatory response
system and by increased oxidative and nitrosative stress.
Nuclear factor kappa beta (NFkappabeta) is the major
upstream, intracellular mechanism which regulates inflammatory
and oxidative stress mediators. In order to examine the role of
NFkappabeta in the pathophysiology of CFS, this study
examines the production of NFkappabeta p50 in unstimulated,
10 ng/mL TNF-alpha (tumor necrosis factor alpha) and 50 ng/mL
PMA (phorbolmyristate acetate) stimulated peripheral blood
lymphocytes of 18 unmedicated patients with CFS and 18
age-sex matched controls.
The unstimulated (F=19.4, df=1/34, p=0.0002),
TNF-alpha-(F=14.0, df=1/34, p=0.0009) and PMA-(F=7.9,
df=1/34, p=0.008) stimulated production of NFkappabeta were
significantly higher in CFS patients than in controls. There were
significant and positive correlations between the production of
NFkappabeta and the severity of illness as measured with the
FibroFatigue scale and with symptoms, such as aches and pain,
muscular tension, fatigue, irritability, sadness, and the subjective
feeling of infection.
The results show that an intracellular inflammatory response in
the white blood cells plays an important role in the
pathophysiogy of CFS and that previous findings on increased
oxidative stress and inflammation in CFS may be attributed to
an increased production of NFkappabeta. The results suggest
that the symptoms of CFS, such as fatigue, muscular tension,
depressive symptoms and the feeling of infection reflect a
genuine inflammatory response in those patients.
It is suggested that CFS patients should be treated with
antioxidants, which inhibit the production of NFkappabeta, such
as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid
and omega-3 fatty acids.
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