Frontiers in Neurology (Nov 2020)

Plasma Inflammatory Cytokines Are Elevated in ALS

  • Rosanna Tortelli,
  • Rosanna Tortelli,
  • Chiara Zecca,
  • Marco Piccininni,
  • Marco Piccininni,
  • Sara Benmahamed,
  • Maria Teresa Dell'Abate,
  • Maria Rosaria Barulli,
  • Rosa Capozzo,
  • Petronilla Battista,
  • Petronilla Battista,
  • Giancarlo Logroscino,
  • Giancarlo Logroscino

DOI
https://doi.org/10.3389/fneur.2020.552295
Journal volume & issue
Vol. 11

Abstract

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease which leads to death in a median time of 2–3 years. Inflammation has been claimed important to the ALS pathogenesis, but its role is still not well-characterized. In the present study, a panel of five cytokines (IL-2, IL-6, IL-10, IFN-gamma, and TNF-alpha) measured in plasma has been investigated in ALS. These biomarkers of inflammation were measured in a population-based cohort of 79 patients with ALS and 79 age- and sex-matched healthy controls using the Bio-Plex technology (Bio-Rad). All the five cytokines were significantly increased in plasma samples of patients compared with controls (p < 0.0001), with IL-6 having the highest median concentration (10.11 pg/ml) in the ALS group. Furthermore, IL-6 was the plasma cytokine with the highest discrimination ability between patients and controls according to the receiver operating characteristic analysis (area under the curve = 0.93). At a cut-off point of 5.71 pg/ml, it was able to classify patients and controls with 91% of sensitivity and 87% of specificity. In the ALS group, plasma IL-6 concentration correlated with demographic (age: rs = 0.25, p = 0.025) and clinical (revised ALS Functional Rating Scale at evaluation: rs = −0.32, p = 0.007; Manual Muscle Testing: rs = −0.33, p = 0.004; progression: rs = 0.29, p = 0.0395) parameters. In line with previous studies, our results confirm that inflammatory cytokines are elevated in ALS, supporting a possible role of inflammation in disease mechanism and progression. However, the precise role of inflammation in ALS needs to be further investigated on larger samples and with more mechanistic studies.

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