Purpose <p>Cigarette smoke (CS) disrupts innate immune homeostasis through oxidative stress and inflammatory signaling, contributing to respiratory diseases such as asthma and COPD. Because <i>Drosophila melanogaster</i> shares approximately 75% of disease-related human genes and possesses a well-characterized innate immune system without confounding adaptive responses, it represents a tractable model for investigating smoke-induced pathology.</p> Methods <p>This study examined the effects of developmental cigarette smoke extract (CSE) exposure on innate immune activation, locomotor activity, and metabolic rate in <i>Drosophila melanogaster</i>.</p> Results <p>Larvae exposed to 10–50% CSE exhibited dose-dependent increases in crystal-cell activation and melanized wound area, indicating heightened innate immune responsiveness likely driven by CSE-induced oxidative stress and hematopoietic dysregulation. Locomotor activity, assessed by negative geotaxis, was impaired at moderate concentrations in both sexes, with females showing greater sensitivity at lower doses, reflecting sex-specific differences. Metabolic rate measurements revealed a significant hypermetabolic response exclusively in male flies at 50% CSE, consistent with an elevated oxidative detoxification burden and vulnerability in males. </p> Conclusion <p>Collectively, these findings demonstrate that CSE elicits a coordinated physiological stress response integrating immune activation with behavioral and metabolic dysfunction. This work supports <i>Drosophila melanogaster</i> as a translational model for dissecting the systemic consequences of smoke-induced innate immune dysregulation.</p>

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Cigarette Smoke Extract Exposure Affects Innate Immune Response, Metabolic Rate, and Locomotor Activity of Drosophila melanogaster

  • Periklis Marnas,
  • Lydia Giannakou,
  • Eleanna Pitaraki,
  • Elpiniki Stergiopoulou,
  • Panagiotis Tzamalas,
  • Athanasios Stefanos Giannopoulos,
  • Maria Anastasia Parlantza,
  • Konstantinos Gourgoulianis,
  • Chrissi Hatzoglou,
  • Erasmia Rouka,
  • Stefan Lüpold,
  • Sotirios G. Zarogiannis

摘要

Purpose

Cigarette smoke (CS) disrupts innate immune homeostasis through oxidative stress and inflammatory signaling, contributing to respiratory diseases such as asthma and COPD. Because Drosophila melanogaster shares approximately 75% of disease-related human genes and possesses a well-characterized innate immune system without confounding adaptive responses, it represents a tractable model for investigating smoke-induced pathology.

Methods

This study examined the effects of developmental cigarette smoke extract (CSE) exposure on innate immune activation, locomotor activity, and metabolic rate in Drosophila melanogaster.

Results

Larvae exposed to 10–50% CSE exhibited dose-dependent increases in crystal-cell activation and melanized wound area, indicating heightened innate immune responsiveness likely driven by CSE-induced oxidative stress and hematopoietic dysregulation. Locomotor activity, assessed by negative geotaxis, was impaired at moderate concentrations in both sexes, with females showing greater sensitivity at lower doses, reflecting sex-specific differences. Metabolic rate measurements revealed a significant hypermetabolic response exclusively in male flies at 50% CSE, consistent with an elevated oxidative detoxification burden and vulnerability in males.

Conclusion

Collectively, these findings demonstrate that CSE elicits a coordinated physiological stress response integrating immune activation with behavioral and metabolic dysfunction. This work supports Drosophila melanogaster as a translational model for dissecting the systemic consequences of smoke-induced innate immune dysregulation.