Neuroinflammation markers and methyl alcohol induced toxic brain damage

0492513 - ÚFCH JH 2019 RIV IE eng J - Článek v odborném periodiku
Zakharov, S. - Hlušička, J. - Nurieva, O. - Kotíková, K. - Lischková, L. - Kačer, P. - Kacerova, T. - Urban, P. - Vaněčková, M. - Seidl, Z. - Diblik, P. - Kuthan, P. - Heissigerová, J. - Lešovský, J. - Rulíšek, J. - Vojtová, L. - Hubáček, J. A. - Navrátil, Tomáš
Neuroinflammation markers and methyl alcohol induced toxic brain damage.
Toxicology Letters. Roč. 298, DEC 2018 (2018), s. 60-69. ISSN 0378-4274. E-ISSN 1879-3169
Institucionální podpora: RVO:61388955
Klíčová slova: CNS damage * Interleukins * Lipoxins * Methyl alcohol poisoning * Neuroinflammation * Non-traumatic brain injury
Obor OECD: Physical chemistry
Impakt faktor: 3.499, rok: 2018

Methyl alcohol intoxication is a global problem with high mortality and long-term visual sequelae and severe brain damage in survivors. The role of neuroinflammation in the mechanisms of methyl alcohol-induced toxic brain damage has not been well studied. We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL-4, IL-5, IL-9, IL-10, and IL-13 in the serum of patients treated with methyl alcohol poisoning and the follow-up concentrations in survivors two years after discharge from the hospital. A series of acute measurements was performed in 28 hospitalized patients (mean age 54.2 ± 5.2 years, mean observation time 88 ± 20 h) and the follow-up measurements were performed in 36 subjects who survived poisoning (including 12/28 survivors from the acute group). Visual evoked potentials (VEP) and magnetic resonance imaging of the brain (MRI) were performed to detect long-term visual and brain sequelae of intoxication. The acute concentrations of inflammatory mediators were higher than the follow-up concentrations: LxA4, 62.0 ± 6.0 vs. 30.0 ± 5.0 pg/mL, LxB4, 64.0 ± 7.0 vs. 34.0 ± 4.0 pg/mL, IL-4, 29.0 ± 4.0 vs. 15.0 ± 1.0 pg/mL, IL-5, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL, IL-9, 30.0 ± 4.0 vs. 13.0 ± 1.0 pg/mL, IL-10, 38.0 ± 5.0 vs. 16.0 ± 1.0 pg/mL, IL-13, 35.0 ± 4.0 vs. 14.0 ± 1.0 pg/mL (all p < 0.001). The patients with higher follow-up IL-5 concentration had prolonged latency P1 (r = 0.413, p = 0.033) and lower amplitude N1P1 (r = −0.498, p = 0.010) of VEP. The higher follow-up IL-10 concentration was associated with MRI signs of brain necrotic damage (r = 0.533, p = 0.001) and brain hemorrhage (r = 0.396, p = 0.020). Our findings suggest that neuroinflammation plays an important role in the mechanisms of toxic brain damage in acute methyl alcohol intoxication.
Trvalý link: http://hdl.handle.net/11104/0286015