Table 1 |
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Overview of the different immune, inflammatory, oxidative and nitrosative stress (IO&NS) aberrations in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) |
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Aberrations in the IO&NS pathways in ME/CFS |
Reference(s) |
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Increased production of key inflammatory mediators, such as NFκB, COX-2, iNOS |
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Increased levels of proinflammatory cytokines |
Fletcher et al. [12] |
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Immune activation, with increased in vivo expression of activation markers, such as CD38, and Th 1-like or Th 2-like responses |
Klimas et al. [13] |
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Immunosuppression, for example, diminished natural killer cell activity (NKCA), and decreased ex vivo expression of activation markers, such as CD69 |
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Depleted antioxidant levels |
Maes et al. [15] |
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Increased levels of radical oxygen (ROS) and nitrogen species (RNS) |
Kennedy et al. [16] |
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Oxidative damage to membrane fatty acids, mitochondria, functional proteins and DNA |
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Autoimmune responses against oxidatively modified fatty acids and nitrated proteins (neoepitopes) |
Maes et al. [9] |
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Autoimmune reactions |
Maes (review) [19] |
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Gut dysbiosis and gut-derived inflammation with increased bacterial translocation |
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Mitochondrial dysfunctions with lower carnitine and coenzyme Q10 levels |
Myhill et al. [24], Plioplys and Plioplys [25], Maes et al. [7] |
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Upregulation and dysregulation of the 2'-5' oligoadenylate synthetase/RNase L pathway |
Nijs and De Meirleir [26] |
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Apoptosis pathways |
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Ion channel dysfunction (channelopathy) |
Broderick et al. [29] |
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Lowered omega-3 polyunsaturated fatty acids |
Maes et al. [30] |
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For space considerations, this table only shows a selection of the relevant references. A more comprehensive listing can be supplied on request from the authors. COX-2: cyclo-oxygenase 2; iNOS = inducible nitric oxide synthase; NFκB = nuclear factor κB; Th = T helper. |
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Maes and Twisk BMC Medicine 2010 8:35 doi:10.1186/1741-7015-8-35 |
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