|
Increased production of key inflammatory mediators, such as NFκB, COX-2, iNOS
|
Maes et al. [10], Maes et al. [11]
|
|
Increased levels of proinflammatory cytokines
|
Fletcher et al. [12]
|
|
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]
|
|
Immunosuppression, for example, diminished natural killer cell activity (NKCA), and decreased ex vivo expression of activation markers, such as CD69
|
Maher et al. [14], Mihaylova et al. [8]
|
|
Depleted antioxidant levels
|
Maes et al. [15]
|
|
Increased levels of radical oxygen (ROS) and nitrogen species (RNS)
|
Kennedy et al. [16]
|
|
Oxidative damage to membrane fatty acids, mitochondria, functional proteins and DNA
|
Maes et al. [17], Behan et al. [18]
|
|
Autoimmune responses against oxidatively modified fatty acids and nitrated proteins (neoepitopes)
|
Maes et al. [9]
|
|
Autoimmune reactions
|
Maes (review) [19]
|
|
Gut dysbiosis and gut-derived inflammation with increased bacterial translocation
|
Maes et al. [20–22], Sheedy et al. [23]
|
|
Mitochondrial dysfunctions with lower carnitine and coenzyme Q10 levels
|
Myhill et al. [24], Plioplys and Plioplys [25], Maes et al. [7]
|
|
Upregulation and dysregulation of the 2'-5' oligoadenylate synthetase/RNase L pathway
|
Nijs and De Meirleir [26]
|
|
Apoptosis pathways
|
Gow et al. [27], Kerr et al. [28]
|
|
Ion channel dysfunction (channelopathy)
|
Broderick et al. [29]
|
|
Lowered omega-3 polyunsaturated fatty acids
|
Maes et al. [30]
|
