C5a complement levels in clinical remission AQP4-IgG-positive NMO patients

Manín, Analisa; Justo, Mariano E; Leoni, Juliana; Paz, Mariela L.; Villa, Andrés

doi:10.1007/s13760-023-02261-7

Cited by 2 publications

(1 citation statement)

References 19 publications

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“…Multiple studies have shown that serum levels of C3 and C4 are lower in NMOSD during acute attacks when compared to controls and patients with MOGAD ( 44 , 45 ). However, in clinically stable patients C3 and C4 trends are inconsistent, with one study showing lower C4 but not C3 ( 46 ), another showing lower C3 but not C4 ( 47 ), and another showing no difference in C3 or C4 when comparing remitted NMOSD patients to controls ( 48 ). Notably, these studies were performed on small cohorts and inconsistent results may be attributable to differences in assay techniques, duration of remission, and disease-modifying therapies.…”

Section: Complementmentioning

confidence: 99%

Soluble biomarkers for Neuromyelitis Optica Spectrum Disorders: a mini review

Rodin,

Chitnis

2024

Front. Neurol.

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The Neuromyelitis Optica Spectrum Disorders (NMOSD) constitute a spectrum of rare autoimmune diseases of the central nervous system characterized by episodes of transverse myelitis, optic neuritis, and other demyelinating attacks. Previously thought to be a subtype of multiple sclerosis, NMOSD is now known to be a distinct disease with unique pathophysiology, clinical course, and treatment options. Although there have been significant recent advances in the diagnosis and treatment of NMOSD, the field still lacks clinically validated biomarkers that can be used to stratify disease severity, monitor disease activity, and inform treatment decisions. Here we review many emerging NMOSD biomarkers including markers of cellular damage, neutrophil-to-lymphocyte ratio, complement, and cytokines, with a focus on how each biomarker can potentially be used for initial diagnosis, relapse surveillance, disability prediction, and treatment monitoring.

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Section: Complementmentioning

confidence: 99%

Soluble biomarkers for Neuromyelitis Optica Spectrum Disorders: a mini review

Rodin,

Chitnis

2024

Front. Neurol.

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C3a Mediates Endothelial Barrier Disruption in Brain-Derived, but Not Retinal, Human Endothelial Cells

Wolf,

Guempelein,

Schikora

et al. 2024

IJMS

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Neuromyelitis optica spectrum disorder (NMOSD) is associated with pathological aquaporin-4 immunoglobulin G (AQP4-IgG), which cause brain damage. However, the impact of AQP4-IgG on retinal tissue remains unclear. Additionally, dysregulated complement anaphylatoxins C3a and C5a, known to modulate the endothelial barrier, are implicated in NMOSD. This study evaluates the susceptibility of human brain microvascular endothelial cells (HBMEC) and human retinal endothelial cells (HREC) to C3a- and C5a-mediated stress using real-time cell barrier analysis, immunocytochemical staining, qPCR and IgG transmigration assays. The findings reveal that C3a induced a concentration-dependent paracellular barrier breakdown and increased transcellular permeability in HBMEC, while HREC maintained barrier integrity under the same conditions. C5a attenuated C3a-induced disruption in HBMEC, indicating a protective role. Anaphylatoxin treatment elevated transcript levels of complement component C3 and increased C5 gene and protein expression in HREC, with no changes observed in HBMEC. In HBMEC, C5a treatment led to a transient upregulation of C3a receptor (C3AR) mRNA and an early decrease in C5a receptor 1 (C5AR1) protein detection. Conversely, HREC exhibited a late increase in C5aR1 protein levels. These results indicate that the retinal endothelial barrier is more stable under anaphylatoxin-induced stress compared to the brain, potentially offering better protection against paracellular AQP4-IgG transport.

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C5a complement levels in clinical remission AQP4-IgG-positive NMO patients

Cited by 2 publications

References 19 publications

Soluble biomarkers for Neuromyelitis Optica Spectrum Disorders: a mini review

Soluble biomarkers for Neuromyelitis Optica Spectrum Disorders: a mini review

C3a Mediates Endothelial Barrier Disruption in Brain-Derived, but Not Retinal, Human Endothelial Cells

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