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<p>Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic interstitial lung disease characterized by aberrant epithelial repair, oxidative stress, and chronic inflammatory activation. Although local pulmonary mechanisms have been extensively investigated, systemic molecular alterations in untreated patients remain incompletely understood. This study aimed to explore circulating inflammatory, redox, apoptosis-related, and repair-associated alterations in drug-naive IPF. In this prospective exploratory case–control study, 35 drug-naive IPF patients and 40 healthy controls were enrolled. IPF diagnosis was established according to multidisciplinary evaluation and current international diagnostic guidelines. Serum levels of IL-6, IL-1β, and IL-18 were measured by ELISA. Oxidative stress parameters, including total oxidant status (TOS), total antioxidant status (TAS), and superoxide dismutase (SOD), were evaluated using colorimetric assays. Expression levels of p53, EGFR, VEGF, BAX, BCL-2, and FGF were analyzed by quantitative real-time PCR. Statistical analyses were performed using the Mann–Whitney U test. Drug-naive IPF patients exhibited significantly elevated circulating IL-6, IL-1β, and IL-18 levels compared with healthy controls (all <i>p</i> &lt; 0.05), indicating systemic inflammatory activation. Oxidative stress analysis demonstrated significantly increased TOS levels together with reduced TAS and SOD activity (all <i>p</i> &lt; 0.05), consistent with systemic redox imbalance. Gene expression analysis revealed significantly increased p53 and VEGF expression, whereas EGFR expression was significantly decreased in the IPF group (<i>p</i> &lt; 0.05). No significant differences were observed for BAX, BCL-2, or FGF expression. Collectively, these findings suggest the presence of coordinated inflammatory, oxidative, and stress-response alterations in untreated IPF. Drug-naive IPF was associated with detectable systemic inflammatory, redox, and apoptosis-related alterations in peripheral blood samples. These findings support the concept that circulating biomarker changes may accompany early IPF pathobiology beyond the local lung environment. However, given the exploratory and peripheral blood-based design of the study, further tissue-level and longitudinal investigations are required to clarify the mechanistic and clinical significance of these observations.</p>

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Circulating inflammatory, redox, and apoptosis-related alterations in drug-naive idiopathic pulmonary fibrosis: an exploratory case–control study

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • İlknur Kaya,
  • Beyza Kaya,
  • Ayşe Koçak Sezgin,
  • Meliha Koldemir Gündüz,
  • Ümran Erbay

摘要

Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic interstitial lung disease characterized by aberrant epithelial repair, oxidative stress, and chronic inflammatory activation. Although local pulmonary mechanisms have been extensively investigated, systemic molecular alterations in untreated patients remain incompletely understood. This study aimed to explore circulating inflammatory, redox, apoptosis-related, and repair-associated alterations in drug-naive IPF. In this prospective exploratory case–control study, 35 drug-naive IPF patients and 40 healthy controls were enrolled. IPF diagnosis was established according to multidisciplinary evaluation and current international diagnostic guidelines. Serum levels of IL-6, IL-1β, and IL-18 were measured by ELISA. Oxidative stress parameters, including total oxidant status (TOS), total antioxidant status (TAS), and superoxide dismutase (SOD), were evaluated using colorimetric assays. Expression levels of p53, EGFR, VEGF, BAX, BCL-2, and FGF were analyzed by quantitative real-time PCR. Statistical analyses were performed using the Mann–Whitney U test. Drug-naive IPF patients exhibited significantly elevated circulating IL-6, IL-1β, and IL-18 levels compared with healthy controls (all p < 0.05), indicating systemic inflammatory activation. Oxidative stress analysis demonstrated significantly increased TOS levels together with reduced TAS and SOD activity (all p < 0.05), consistent with systemic redox imbalance. Gene expression analysis revealed significantly increased p53 and VEGF expression, whereas EGFR expression was significantly decreased in the IPF group (p < 0.05). No significant differences were observed for BAX, BCL-2, or FGF expression. Collectively, these findings suggest the presence of coordinated inflammatory, oxidative, and stress-response alterations in untreated IPF. Drug-naive IPF was associated with detectable systemic inflammatory, redox, and apoptosis-related alterations in peripheral blood samples. These findings support the concept that circulating biomarker changes may accompany early IPF pathobiology beyond the local lung environment. However, given the exploratory and peripheral blood-based design of the study, further tissue-level and longitudinal investigations are required to clarify the mechanistic and clinical significance of these observations.