Brenu/Marshall:

 

ME/CVS

gaat gepaard met

slechte werkzaamheid

van NK-cellen en neutrofielen

 

 

 

 


 

Brenu en kollega's hebben onderzoek uitgevoerd naar de immunologische afwijkingen

bij 10 ME/CVS-patiŽnten (lang ziek) en 10 gezonde medemensen.

 

De grootste verschillen tussen patiŽnten en gezonde proefpersonen::

  • verminderde werkzaamheid van NK-cellen (cytotoxiciteit: vermogen om te doden)
  • verminderde vernietigingskracht van neutrofielen (afgifte van vrije radikalen, klik hier)
  • lagere aantallen "regulerende" NK cellen (CD56brightCD16-).

Opvallend is voorts dat de onderzoekers geen verschillen in de (relatieve) aantallen van de verschillende witte bloedcellen en geen bloedcelafwijkingen geconstateerd hebben.

 

Wellicht heeft dit te maken met de omvang van de steekproef (10!) en

het feit dat de onderzochte patiŽnten al langer ziek waren.

 

Tot slot een vraag aan vermoeidheids-en-stressdeskundigen:

Kunnen we die NK-cellen en neutrofiele granulocyten niet naar gedragstherapie sturen?

 

 


 

Enkele citaten uit het uitgebreide studierapport:

 

 

Altered distribution of NK phenotypes

 

CD56brightCD16- NK lymphocytes were significantly reduced ...

in CFS patients ... compared to controls ....

 

CD56dimCD16+ did not statistically differ between groups ....

 

CD56brightCD16- NK cells

preferentially secrete high levels of cytokines and have limited cytotoxic function

while CD56dimCD16+ NK cells are mainly cytotoxic [11].

 

 

Decreased NK cytotoxic activity

 

NK cytotoxic activity

was measured by assessing

the ability of NK lymphocytes

from the healthy subjects and the control group

to induce apoptosis in K562.

 

The percentage lysis

for the healthy subjects and the CFS patients

were significantly different.

 

 

Impaired neutrophil function

 

... in the healthy subjects...

a significantly higher amount of neutrophils

are affirmative for intracellular oxidation of E. coli,

while in the CFS patients ...

significantly lower levels of neutrophils

were positive for oxidative burst after phagocytising the E. coli ....

 

 

 

Discussion

 

Diminishing levels of CD56brightCD16- NK cells

may limit the production of TNFs,

cytokines required for activation of respiratory burst in neutrophils.

 

These deficiencies in NK activity

may increase viral load in CFS,

incidentally a recent study observed

increases in xenotropic murine leukemia virus-related virus (XMRV)

in peripheral blood samples of CFS patients [47].

 

These viruses

may potentially alter aspects of the immune response such as cytotoxic activity

thus promoting their survival

in particular immune cells.

 

 


 

Immune and hemorheological changes in Chronic Fatigue Syndrome

Journal of Translational Medicine 2010, 8:1doi:10.1186/1479-5876-8-1

Ekua W Brenu, Donald R Staines, Oguz K Baskurt, Kevin J Ashton, Sandra B Ramos, Rhys M Christy and Sonya M Marshall-Gradisnik

 

 

Published: 11 January 2010

 

Abstract (provisional)

 

Background

 

Chronic Fatigue Syndrome (CFS) is a multifactorial disorder

that affects various physiological systems including immune and neurological systems.

 

The immune system has been substantially examined in CFS with equivocal results,

however, little is known about the role of neutrophils and natural killer (NK) phenotypes

in the pathomechanism of this disorder.

 

Additionally,

the role of erythrocyte rheological characteristics in CFS has not been fully expounded.

 

The objective of this present study was to determine

deficiencies in lymphocyte function and erythrocyte rheology in CFS patients.

 

 

Methods

 

Flow cytometric measurements were performed for

neutrophil function, lymphocyte numbers,

NK phenotypes (CD56dimCD16+ and CD56brightCD16-) and NK cytotoxic activity.

 

Erythrocyte aggregation, deformability and fibrinogen levels were also assessed.

 

 

Results

 

CFS patients (n = 10) had

significant decreases in

neutrophil respiratory burst,

NK cytotoxic activity and

CD56brightCD16- NK phenotypes

in comparison to healthy controls (n = 10).

 

However,

hemorheological characteristics, aggregation, deformability and fibrinogen,

lymphocyte numbers and CD56dimCD16+ NK cells

were similar between groups.

 

 

Conclusion

 

Immune dysfunction

may therefore be

an important contributory factor to the mechanism of CFS,

as indicated by

decreases in neutrophil respiratory burst, NK cell activity and NK phenotypes.

 

Thus,

immune cell function and phenotypes

are possible diagnostic markers

for CFS.

 

 

http://www.translational-medicine.com/content/pdf/1479-5876-8-1.pdf

 

 


 

Met dank aan Brigitte, Rob en Dean die me op deze studie opmerkzaam maakten.