Characteristics of serum Metrnl levels in patients with neuromyelitis optica spectrum disorder and their…

Abstract

Background: Neuromyelitis optica spectrum disorder (NMOSD) is a severe autoimmune inflammatory disease for which reliable biomarkers of disease activity are lacking. Meteorin-like protein (Metrnl) has not been investigated in NMOSD; this study assessed its clinical significance in NMOSD patients.

Methods: Serum Metrnl, interleukin (IL)-6, and IL-17A levels were quantified by enzyme-linked immunosorbent assay in 50 patients with NMOSD and 30 age- and sex-matched healthy controls (HCs) and correlated with clinical and laboratory data. Metrnl levels were also remeasured in 30 patients before and after high-dose methylprednisolone therapy, together with derived inflammatory indices. Benjamini–Hochberg false-discovery-rate (FDR) correction was applied within prespecified test families, with a sensitivity power analysis. Metrnl alone and a combined multimarker logistic regression model were evaluated by receiver operating characteristic (ROC) analysis, DeLong tests, bootstrap validation, calibration, and decision curve analysis.

Results: Serum Metrnl levels were higher in NMOSD patients than in HCs and were greater in those with mild disability than in those with moderate-to-severe disability (both p < 0.001); the increase in patients with gadolinium-enhancing lesions was nominal ( p = 0.034, q = 0.068). After FDR correction, serum Metrnl levels correlated negatively with IL-6, IL-17A, neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), and Expanded Disability Status Scale (EDSS) score (all q < 0.05), but not with high-sensitivity C-reactive protein (hs-CRP). Metrnl alone distinguished NMOSD patients from HCs (area under the curve [AUC] 0.752), whereas a combined model of Metrnl, IL-6, IL-17A, and hs-CRP performed markedly better (AUC 0.933; DeLong p < 0.001), increasing specificity from 53.3% to 80.0% at 100% sensitivity. After methylprednisolone therapy, Metrnl, IL-6, and IL-17A levels decreased ( p < 0.001) along with clinical improvement, whereas NLR, platelet-to-lymphocyte ratio, and SII remained unchanged; the decrease in Metrnl levels (median −25.5%) was the largest and was uncorrelated with changes in other biomarkers.

Conclusions: Serum Metrnl levels were elevated in patients with NMOSD, inversely related to disease severity and inflammatory biomarkers, and decreased after immunotherapy, supporting it as a dynamic biomarker of disease activity and a component of a multimarker diagnostic panel. The cross-sectional design precludes causal inference, and exploratory subgroup findings require external validation.

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BibTeX

@article{li2026characteristics,
  title = {{Characteristics of serum Metrnl levels in patients with neuromyelitis optica spectrum disorder and their associations with disease activity and inflammatory biomarkers}},
  author = {Li-Min Li and Yingzhe Shao and Hao Cai and Li Yang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1957990},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1957990/full},
  note = {CC BY 4.0},
}

RIS

TY  - JOUR
TI  - Characteristics of serum Metrnl levels in patients with neuromyelitis optica spectrum disorder and their associations with disease activity and inflammatory biomarkers
AU  - Li-Min Li
AU  - Yingzhe Shao
AU  - Hao Cai
AU  - Li Yang
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1957990
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1957990/full
AB  - Background: Neuromyelitis optica spectrum disorder (NMOSD) is a severe autoimmune inflammatory disease for which reliable biomarkers of disease activity are lacking. Meteorin-like protein (Metrnl) has not been investigated in NMOSD; this study assessed its clinical significance in NMOSD patients.  Methods: Serum Metrnl, interleukin (IL)-6, and IL-17A levels were quantified by enzyme-linked immunosorbent assay in 50 patients with NMOSD and 30 age- and sex-matched healthy controls (HCs) and correlated with clinical and laboratory data. Metrnl levels were also remeasured in 30 patients before and after high-dose methylprednisolone therapy, together with derived inflammatory indices. Benjamini–Hochberg false-discovery-rate (FDR) correction was applied within prespecified test families, with a sensitivity power analysis. Metrnl alone and a combined multimarker logistic regression model were evaluated by receiver operating characteristic (ROC) analysis, DeLong tests, bootstrap validation, calibration, and decision curve analysis.  Results: Serum Metrnl levels were higher in NMOSD patients than in HCs and were greater in those with mild disability than in those with moderate-to-severe disability (both p &lt; 0.001); the increase in patients with gadolinium-enhancing lesions was nominal ( p = 0.034, q = 0.068). After FDR correction, serum Metrnl levels correlated negatively with IL-6, IL-17A, neutrophil-to-lymphocyte ratio (NLR), systemic immune-inflammation index (SII), and Expanded Disability Status Scale (EDSS) score (all q &lt; 0.05), but not with high-sensitivity C-reactive protein (hs-CRP). Metrnl alone distinguished NMOSD patients from HCs (area under the curve [AUC] 0.752), whereas a combined model of Metrnl, IL-6, IL-17A, and hs-CRP performed markedly better (AUC 0.933; DeLong p &lt; 0.001), increasing specificity from 53.3% to 80.0% at 100% sensitivity. After methylprednisolone therapy, Metrnl, IL-6, and IL-17A levels decreased ( p &lt; 0.001) along with clinical improvement, whereas NLR, platelet-to-lymphocyte ratio, and SII remained unchanged; the decrease in Metrnl levels (median −25.5%) was the largest and was uncorrelated with changes in other biomarkers.  Conclusions: Serum Metrnl levels were elevated in patients with NMOSD, inversely related to disease severity and inflammatory biomarkers, and decreased after immunotherapy, supporting it as a dynamic biomarker of disease activity and a component of a multimarker diagnostic panel. The cross-sectional design precludes causal inference, and exploratory subgroup findings require external validation.
SN  - 1664-3224
ER  -

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