Circulating α-Klotho Is Positively Associated with Eosinophil Counts in Community-Dwelling Older Adults: A Cross-Sectional Study

Biology, 2026

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DOI 10.3390/biology15211916
Достоверность данных 70 средняя
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Аннотация

Background: The relation of circulating α-Klotho to individual leukocyte populations is uncertain. An exploratory 13-marker hematological screen identified eosinophils as a candidate signal, motivating this focused analysis. Methods: The grant-funded α-Klotho substudy included 504 assayed serum specimens. After excluding one participant aged < 60 years and one with missing age, 502 participants were eligible. α-Klotho was measured with the FineTest Human SAKL ELISA kit (EH4278; calibration range 93.75–6000 pg/mL). Because results above the upper calibrator had been software-extrapolated without repeat dilution, the primary analysis was restricted to 397 participants with reported concentrations ≤ 6000 pg/mL; 388 had an eosinophil count. Spearman’s correlations were corrected across 13 hematological markers using Benjamini–Hochberg adjustment. Ordinary least-squares models used HC3 heteroskedasticity-consistent standard errors. Results: Median α-Klotho in the primary cohort was 1179.67 pg/mL (IQR 920.07–1686.51). Absolute eosinophil count correlated weakly with α-Klotho (ρ = 0.120; p = 0.018), but the association did not survive correction across the screening family (q = 0.146). In the fully adjusted model (n = 376), each 1 SD higher log-eosinophil count was associated with 8.4% higher α-Klotho (95% CI 2.0–15.2%; p = 0.009). The quartile trend was significant (p = 0.019), whereas median regression produced a smaller estimate (5.4%; bootstrap 95% CI −0.6 to 12.5%). Estimates were similar after recruitment-stratum adjustment and after excluding eosinophilia, chronic respiratory disease, or leukocyte counts > 15 × 109/L. Conclusions: Within the assay calibration range, higher eosinophil counts were associated with modestly higher serum α-Klotho after adjustment for measured covariates. The post hoc origin, assay limitations, and cross-sectional design make this a hypothesis-generating immune association rather than evidence of causality, healthy longevity, or a clinical threshold.