Table 1.

Selected references showing evidence of systemic mediators and iron dysregulation of inflammation in Parkinson’s disease.

Mediators of Inflammation	References
Presence of activated microglia, dysregulated inflammatory mediators, chemokines, oxidative stress, and both systemic and CNS inflammation	[54,83,84,85,86,87]
Presence of dysregulated cytokines, including interleukin (IL)-1β, IL-2, IL-6, IL-10, tumour necrosis factor (TNF)-α, interferon (IFN)γ, RANTES), and C-reactive protein (CRP)	[45,88,89,90,91,92,93]
Increased cluster of differentiation (CD) 4+ T-cells indicating peripheral lymphocyte activation	[94,95]
Presence of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2) in postmortem PD brains	[96,97]
Increase in gut–brain axis and intestinal inflammation. An increase in enteric inflammation associated with increased mRNA and mRNA that are associated with glial markers	[10,42,43,98,99]
Increased presence of stool immune factors	[100,101]
Dysregulated bacterial inflammagens like LPS (lipopolysaccharides) and bacterial proteases like gingipains	[45,102,103,104]
Iron dysregulation	[20,50,62,63,105,106,107,108,109,110,111,112,113,114,115]