Scholarlink

Background <p>Physical frailty is a prevalent geriatric syndrome associated with reduced physiological resilience and adverse outcomes. Beyond classical inflammaging, age-related changes in immune regulation and tissue repair may contribute to frailty pathophysiology. Biomarkers involved in adaptive immune responses and remodeling pathways, such as IL-17 and TGF-β1, may help characterize the inflammatory-regenerative milieu associated with frailty. We therefore investigated the association between circulating immune biomarkers and physical frailty severity in older adults.</p> Methods <p>In this cross-sectional analysis, 167 community-dwelling outpatients aged ≥ 65&#xa0;years (mean age 75.2 ± 6.4&#xa0;years; 54.5% women) were classified as robust, pre-frail, or frail according to a phenotype-based frailty score. Circulating levels of TGF-β1, IL-17, IL-6, TNF-α, IL-10, and IFN-γ were measured. Associations with frailty were assessed using ordinal logistic regression, quantile regression, and component-specific logistic models.</p> Results <p>IL-17 concentrations progressively declined with increasing frailty severity (median 9.24&#xa0;ng/L in robust vs. 4.91&#xa0;ng/L in frail participants; <i>p</i> = 0.004). In adjusted ordinal models, higher IL-17 levels were independently associated with lower frailty severity (OR = 0.62, 95% CI 0.46–0.84; <i>p</i> = 0.002), with each doubling of IL-17 corresponding to a 28% reduction in frailty odds. Conversely, higher TGF-β1 levels were independently associated with greater frailty severity (OR = 2.33, 95% CI 1.05–5.13; <i>p</i> = 0.036). IL-17 showed consistent associations with physical frailty domains, including slowness (adjusted OR = 0.57), and low physical performance (adjusted OR = 0.68). Similar associations were observed in exploratory analyses restricted to cognitively intact participants. However, formal interaction analyses did not support significant effect modification by cognitive status. In contrast, classical inflammatory markers (IL-6, TNF-α), as well as IFN-γ and IL-10, were not significantly associated with frailty across any of the models.</p> Conclusions <p>Physical frailty was associated with lower IL-17 and higher TGF-β1 levels, suggesting that immune-related pathways beyond classical systemic inflammation may be associated with physical frailty. Rather than reflecting overt systemic inflammation, these findings suggest that biological pathways involved in immune regulation and tissue remodeling may be associated with physical frailty. IL-17 and TGF-β1 may therefore represent potentially informative biomarkers for future investigations of the biological mechanisms underlying resilience and functional decline in aging.</p> Trial registration <p>Not applicable.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Associations of IL-17 and TGF-β1 with physical frailty in older adults

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月4日

查看全文
  • Chiara Ceolin,
  • Marina De Rui,
  • Giulia Musso,
  • Silvia Sturani,
  • Adele Ravelli,
  • Cristina Simonato,
  • Franz Villanova,
  • Sabrina Pigozzo,
  • Luca Busetto,
  • Angelo Antonini,
  • Eleonora Fiorenzato,
  • Martina Montagnana,
  • Alessandra Coin,
  • Maria Devita,
  • Giuseppe Sergi,
  • Filippo Augusto Barbini,
  • Silvia Bettini,
  • Carlotta Bortoluzzi,
  • Simone Cauzzo,
  • Marta Conforti,
  • Alessandra Giannella,
  • Gabriella Milan,
  • Stefania Moz,
  • Maria Laura Nasi,
  • Anna Pilatone,
  • Catia Pilon,
  • Claudia Maria Radu,
  • Milena Spoa

摘要

Background

Physical frailty is a prevalent geriatric syndrome associated with reduced physiological resilience and adverse outcomes. Beyond classical inflammaging, age-related changes in immune regulation and tissue repair may contribute to frailty pathophysiology. Biomarkers involved in adaptive immune responses and remodeling pathways, such as IL-17 and TGF-β1, may help characterize the inflammatory-regenerative milieu associated with frailty. We therefore investigated the association between circulating immune biomarkers and physical frailty severity in older adults.

Methods

In this cross-sectional analysis, 167 community-dwelling outpatients aged ≥ 65 years (mean age 75.2 ± 6.4 years; 54.5% women) were classified as robust, pre-frail, or frail according to a phenotype-based frailty score. Circulating levels of TGF-β1, IL-17, IL-6, TNF-α, IL-10, and IFN-γ were measured. Associations with frailty were assessed using ordinal logistic regression, quantile regression, and component-specific logistic models.

Results

IL-17 concentrations progressively declined with increasing frailty severity (median 9.24 ng/L in robust vs. 4.91 ng/L in frail participants; p = 0.004). In adjusted ordinal models, higher IL-17 levels were independently associated with lower frailty severity (OR = 0.62, 95% CI 0.46–0.84; p = 0.002), with each doubling of IL-17 corresponding to a 28% reduction in frailty odds. Conversely, higher TGF-β1 levels were independently associated with greater frailty severity (OR = 2.33, 95% CI 1.05–5.13; p = 0.036). IL-17 showed consistent associations with physical frailty domains, including slowness (adjusted OR = 0.57), and low physical performance (adjusted OR = 0.68). Similar associations were observed in exploratory analyses restricted to cognitively intact participants. However, formal interaction analyses did not support significant effect modification by cognitive status. In contrast, classical inflammatory markers (IL-6, TNF-α), as well as IFN-γ and IL-10, were not significantly associated with frailty across any of the models.

Conclusions

Physical frailty was associated with lower IL-17 and higher TGF-β1 levels, suggesting that immune-related pathways beyond classical systemic inflammation may be associated with physical frailty. Rather than reflecting overt systemic inflammation, these findings suggest that biological pathways involved in immune regulation and tissue remodeling may be associated with physical frailty. IL-17 and TGF-β1 may therefore represent potentially informative biomarkers for future investigations of the biological mechanisms underlying resilience and functional decline in aging.

Trial registration

Not applicable.