Klimas

over (chronische) infekties, ontsteking,

het afweersysteem en de HPA-as.

 

(overzichtsstudie)

 

 

 

 

 

Onlangs verscheen een artikel van de hand van Klimas en O'Brien Koneru

waarin een overzicht gegeven wordt van de huidige stand van zaken

m.b.t. de rol van infekties, ontregeling van het afweersysteem en de HPA-as.

 

 

Enkele belangrijke konstateringen uit deze studie:

 

M.b.t. (de rol van) infekties

  • Er zijn veel studies die wijzen op (een) chronische infektie(s)

    • Enkele recente genenaktiviteitstudies wijzen er op dat

    infekties de ziekte veroorzaken en in stand houden.

  • Niet de persoonlijkheidsstijl, maar de ernst van de infektie bepaalt of iemand ME/CVS "krijgt", als het gaat om specifieke infekties (klik hier).

M.b.t. het afweersysteem

  • De Th1-Th2-balans is verstoord (Th1-> Th2 shift, klik hier)
  • NK- en cytotoxische T-cellen ("wapens" Th1-reaktie) zijn verzwakt.

M.b.t. de HPA-as

  • Een verminderde werking van de HPA-as (wat is de oorzaak?, FT) leidt (in het begin) tot een versterkte stressresponse/reaktie afweersysteem.
  • Langdurige stress (bijv. als gevolg van infekties en spanningen) leidt tot permanente produktie van stresshormonen, die de afweer onderdrukken.

 

 

 

Citaten uit het volledige studierapport

 

 

The homeostasis between the cell-mediated or T helper 1 (Th1) immune response and the humoral or Th2 immune response is disrupted in CFS.

 

 

A large body of evidence links CFS to a persistent viral infection.

 

 

Hypofunctioning of the HPA axis could lead to an exaggerated stress response and a subsequently excessive release of proinflammatory cytokines.

Long-term stress increases levels of glucocorticoids and catecholamines, which over time suppress immune function.

 

 

… CFS patients exhibited a distinct immune profile compared with severely fatigued and nonfatigued individuals. These patients displayed increased anti-inflammatory cytokines (interleukin [IL-10, decreased interferon IFN-gamma / IL-10 ratio) and reductions in pro-inflammatory cytokines (IL-6, tumor necrosis factor-alfa).

 

 

In [a] recent study Hickie et al. demonstrated that CFS is a fairly common sequel of several types of viral and nonviral infections including EBV, Q fever, and Ross River virus. ….. The best predictor of prolonged fatigue was the severity of the acute infection. Premorbid mood disorders and other potential psychiatric risks were not predictive of risk for prolonged fatigue.

 

 

Recent studies using microarray technology have suggested that infectious agents may trigger and perpetuate CFS symptoms.

 

 

Immune dysregulation has been described by many groups, with evidence of cellular dysfunction and chronic immune activation described in early articles on CFS…..

 

 

Patients with CFS often have reduced natural killer cell cytotoxic activity.

 

 

Siegel et al. found that relative to CFS patients with normal NKCA, patients with low NKCA levels reported more cognitive dysfunction, more daytime impairment, and less vigor. These patients also scored lower on objective measures of cognitive function relative to patients with normal NKCA levels.

 

 

The preponderance of available research confirms that immune dysregulation is a primary characteristic of CFS. New research has further elucidated our understanding of the genomics of the illness and the role of viral infection and reactivation in the pathogenesis.

 

 

 

 

Samenvatting

 

 

Chronic fatigue syndrome:

Inflammation, immune function, and neuroendocrine interactions

Current Rheumatology Reports, Volume 9, Number 6, 2007, 482-487.

NG Klimas, A O’Brien Koneru.

 

 

Investigations into the underlying cause of chronic fatigue syndrome have advanced the field considerably in the past year. Gene microarray data have led to a better understanding of pathogenesis. Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments. Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue. Genomic studies showed that persistent cases express Epstein Barr virus-specific genes and demonstrate abnormalities of mitochondrial function. Studies of immune dysfunction extended observations of natural killer cytotoxic cell dysfunction of the cytotoxic T cell through quantitative evaluation of intracellular perforins and granzymes. Other research has focused on a subgroup of patients with reactivated viral infection. These advances should result in targeted therapies that impact immune function, hypothalamic-pituitary-adrenal axis regulation, and persistent viral reactivation.

 

 

bron:

http://www.springerlink.com/content/1535x16058474m11