Serum Immunoglobulin G of Neuro-Behçet’s Disease Patients Reduce Cerebral Expression Levels of Survival Pathway Factors


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Erdağ E., Şahin-Özkartal C., Küçükali C. İ., Arıcıoğlu F., Tüzün E.

NEUROLOGICAL SCIENCES AND NEUROPHYSIOLOGY, vol.37, no.3, pp.118-123, 2020 (SCI-Expanded)

  • Publication Type: Article / Article
  • Volume: 37 Issue: 3
  • Publication Date: 2020
  • Doi Number: 10.4103/nsn.nsn_2_20
  • Journal Name: NEUROLOGICAL SCIENCES AND NEUROPHYSIOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.118-123
  • Istanbul University Affiliated: Yes

Abstract

Objective: Anti-neuronal antibodies are found in sera of neuro-Behçet’s

disease (NBD) patients. In this study, our aim was to analyze the potential

mechanisms by which NBD immunoglobulin (Ig) Gs affect neuronal

dysfunction. Materials and Methods: Purified IgGs obtained from pooled

sera of six each NBD patients and healthy controls (HCs) were administered

to Sprague Dawley rats through intraventricular injection. Control rats received

phosphate-buffered saline (PBS) only. Locomotor activity was assessed by

open field test on days 0, 10, and 25. Cerebral expression levels of intracellular

pathway factors associated with cell survival and viability were measured by

real-time polymerase chain reaction. Results: Rats treated with NBD IgG

exhibited reduced motor activity. On day 25, the mean number of crossings was

44 ± 7, 90 ± 12, and 93 ± 5 and the mean number of rearings was 18 ± 7,

34 ± 5, and 35 ± 6 for NBD IgG, HC IgG, and PBS groups, respectively

(P < 0.001). Relative expression levels of Akt-1 (0.4 ± 0.2, 1.0 ± 0.3, and

0.9 ± 0.6; P = 0.004), DJ-1 (0.6 ± 0.2, 1.0 ± 0.6, and 0.9 ± 0.5; P = 0.047),

mouse double mininute-2 (0.5 ± 0.3, 0.9 ± 0.2, and 1.0 ± 0.2; P = 0.002), and

mechanistic target of rapamycin (0.4 ± 0.2, 0.8 ± 0.4, and 0.9 ± 0.6; P = 0.006)

were significantly lower in NBD-IgG group than HC IgG and PBS groups. By

contrast, the expression levels of factors associated with apoptosis (caspase 3,

mitochondrial carrier homolog 1, and B-cell lymphoma-2) were comparable

among different treatment arms. Conclusion: Our results suggest that at least a

fraction of NBD IgG interacts with neuronal surface antigens and subsequently

decreases neuronal viability through Akt pathway inhibition. By contrast, NBD

IgG does not appear to activate neuronal apoptosis. Further identification of the

binding sites of serum IgG ıs required.