Evaluation of Interleukins, ACTH, Cortisol and Prolactin Concentrations in the Blood of Patients with Parkinson's Disease

Abstract

Parkinson''s disease (PD) is characterized by a markedly decreased number of nigrostriatal dopaminergic neurons. The pathogenesis of PD is still unknown; among other etiological factors, immunological abnormalities have been suggested. Recently, interleukin-2 (IL-2) has been hypothesized to be an endogenous cytokine that regulates striatal dopaminergic function. We examined the plasma concentrations of IL-1, IL-2, IL-6 and blood levels of ACTH, Cortisol and prolactin of 21 patients with PD without any previous treatment. Age-and sex-matched subjects without any neurological or immune disorders were used as controls. Significantly higher serum concentrations of IL-2 in patients with PD were found. Treatment with antiparkinsonian drugs reduced IL-2 levels in these patients. Our results suggest a functional relationship between central dopaminergic and immune systems and a possible involvement of the latter in the pathogenesis of PD.

Contributions of central and systemic inflammation to the pathophysiology of Parkinson's disease

“…Amplified levels of the cytokines TNF-α, IL-2, IL-6 and RANTES (Brodacki et al, 2008;Dobbs et al, 1999;Rentzos et al, 2007;Stypula et al, 1996) have also been detected in serum obtained from PD patients. It has been proposed that increases in these serum cytokine levels may serve as a therapeutic marker for PD, based on a blood sample study of men with high plasma concentrations of IL-6 correlating with an increased risk of developing PD (Chen et al, 2008b).…”

“…Proinflammatory cytokines IL-1β, TNF-α, IL-2, IL-6 and IFN are constitutively expressed at basal levels in PD patients as demonstrated in post-mortem brains, serum and cerebrospinal fluid in vivo (Boka et al, 1994;Dobbs et al, 1999;Mogi et al, 1994a, b;Mount et al, 2007;Stypula et al, 1996). Moreover, the death signalling receptor TNF receptor type-1 (TNFR-1) 9 is expressed on dopaminergic neurons in human SNpc (Boka et al, 1994;Mogi et al, 2000).…”

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

“…A few studies also reported altered levels of serum inflammatory markers in PD patients [552][553][554]. In rats, chronic infusion of bacterial endotoxin lipopolysacharide (LPS) into substantia nigra resulted in activation of microglia followed by degeneration of dopaminergic neurons [555], suggesting that inflammation may precede neurodegeneration.…”

Inflammation in Parkinson’s Disease: Causes and Consequences

“…In support of a role for systemic immune cells in the degeneration of nigral DA neurons, CD4 -/-mice have been shown to be resistant to MPTP-induced neurotoxicity in the SN (Brochard et al, 2009). Amplified TNF , IL-2, IL-6 and RANTES (Brodacki et al, 2008;Dobbs et al, 1999;Rentzos et al, 2007;Stypula et al, 1996) levels have also been detected in serum obtained from PD patients. Increases in serum cytokines may serve as a therapeutic marker for PD as a blood sample study of men with high plasma concentrations of IL-6 revealed an increased risk of developing PD (H. .…”

“…Cytokines produced by LPS-stimulated microglia can potentiate microglial activation through autocrine signalling to create a self-propagating cycle of expression. Pro-inflammatory cytokines IL-1 , TNF , IL-2 and IL-6 are constitutively expressed at basal levels in PD patients as evidenced in post-mortem, serum and cerebrospinal fluid in vivo (Boka et al, 1994;Dobbs et al, 1999;Mogi et al, 1994a;Mogi et al, 1994b;Stypula et al, 1996). Moreover, the death signalling receptor TNF receptor type-1 (TNFR-1) is expressed on DA neurons in human SNpc (Boka et al, 1994;Mogi et al, 2000).…”