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The HMGB 1 is increased in CSF of patients with an Anti‐ NMDAR encephalitis
Author(s) -
Ai P.,
Zhang X.,
Xie Z.,
Liu G.,
Liu X.,
Pan S.,
Wang H.
Publication year - 2018
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.12850
Subject(s) - nmda receptor , chemistry , medicine , receptor , biochemistry
Background Anti‐N‐methyl‐D‐aspartate receptor ( NMDAR ) encephalitis is an autoimmune disorder of the central nervous system ( CNS ). Interleukin ( IL )‐6 and IL ‐17A may play important roles in the pathogenesis of this disease. High‐mobility group box protein 1 ( HMGB 1), a small but highly conserved ubiquitous protein, is recognized to be a potent innate inflammatory mediator that can activate the nuclear factor light chain enhancer of activated B cells and release cytokines such as IL ‐6 and IL ‐17A when released extracellularly. However, whether cerebrospinal fluid ( CSF ) HMGB 1 levels are altered in anti‐ NMDAR encephalitis is still unclear. Objective The aim of this study was to determine whether a correlation exists between the CSF concentrations of HMGB 1 and IL ‐6 and IL ‐17A in anti‐ NMDAR encephalitis patients. We also sought to assess whether HMGB 1 influences the clinical outcomes in anti‐ NMDAR encephalitis patients. Methods Thirty‐three patients with anti‐ NMDAR antibodies and 38 controls were recruited. CSF HMGB 1 was measured using an enzyme‐linked immunosorbent assay. The main clinical outcomes were evaluated using the modified Rankin scale ( mRS ). The data were extracted using microarray analysis software. Results and Conclusion Our results showed significant increases in CSF HMGB 1, IL ‐6, and IL ‐17A ( P < .05) in anti‐ NMDAR encephalitis patients. But between 3 months’ mRS scores in anti‐ NMDAR encephalitis patients and CSF data, there was no correlation. Our study suggests that HMGB 1 CSF levels are increased in patients with anti‐ NMDAR encephalitis and reflect the underlying neuroinflammatory process.