• Medientyp: E-Artikel
  • Titel: Increased Levels of Serum IL-18 Are Associated with the Long-Term Outcome of Severe Traumatic Brain Injury
  • Beteiligte: Ciaramella, Antonio; Della Vedova, Cecilia; Salani, Francesca; Viganotti, Mara; D'Ippolito, Mariagrazia; Caltagirone, Carlo; Formisano, Rita; Sabatini, Umberto; Bossù, Paola
  • Erschienen: S. Karger AG, 2014
  • Erschienen in: Neuroimmunomodulation
  • Sprache: Englisch
  • DOI: 10.1159/000354764
  • ISSN: 1021-7401; 1423-0216
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  • Beschreibung: <jats:p>&lt;b&gt;&lt;i&gt;Objective:&lt;/i&gt;&lt;/b&gt; A long-lasting neuroinflammatory cascade may lead to the progression of brain damage, favoring neurodegeneration and cognitive impairment in patients with traumatic brain injury (TBI), but the potential mechanisms underlying this sequence of events remain elusive. Here we aimed to evaluate the impact of interleukin (IL)-18, a proinflammatory cytokine elevated in post-acute head injury and associated with neurodegeneration, on the long-term outcome of patients with chronic TBI. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; The serum content of IL-18 was evaluated in 16 patients with severe TBI, during their rehabilitation phase, and in a matched group of 16 healthy controls. The disability of the enrolled patients was evaluated by means of the Glasgow Outcome Scale, Levels of Cognitive Functioning, and the Disability Rating Scale. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; The circulating levels of IL-18 were significantly increased in chronic TBI patients, as compared to healthy subjects, and correlated with the patients' cognitive impairment and disability severity. &lt;b&gt;&lt;i&gt;Conclusions:&lt;/i&gt;&lt;/b&gt; IL-18 may contribute to the long-term outcome and neurodegeneration in TBI patients. Even though further studies are needed to understand the molecular mechanisms underlying the effects of IL-18 on TBI progression and its associated drop in cognitive function, a possible role of this cytokine as a therapeutic target in TBI can be envisaged.</jats:p>