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Related Experiment Video

Updated: Nov 18, 2025

Author Spotlight: Developing a Microfluidic Lung-on-Chip Model for In-Depth Study of Human Immune Response and Infection Mechanisms
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Novel three-dimensional biochip pulmonary sarcoidosis model.

Tess M Calcagno1, Chongxu Zhang2, Runxia Tian2

  • 1Department of Medicine, University of Miami, Miami, FL, United States of America.

Plos One
|February 4, 2021
PubMed
Summary

Researchers developed a novel 3D biochip model to study sarcoidosis, a lung disorder. This innovative model mimics granuloma formation, offering new insights into the disease's pathogenesis and potential treatments.

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Area of Science:

  • Biomedical Engineering
  • Pulmonary Medicine
  • Inflammation Research

Background:

  • Sarcoidosis is a complex multi-system inflammatory disease primarily affecting the lungs, with poorly understood etiology and pathogenesis.
  • Current research is limited by the lack of reliable in vitro models that accurately replicate sarcoidosis pathology, particularly granuloma formation.
  • Developing advanced models is crucial for advancing our understanding and therapeutic strategies for sarcoidosis.

Purpose of the Study:

  • To develop an in vitro three-dimensional (3D) lung-on-chip biochip model that mimics granuloma formation in sarcoidosis.
  • To create a novel pulmonary sarcoidosis model using patient-derived granulomas within a microfluidic lung-on-membrane system.
  • To investigate the inflammatory cytokine response within this new 3D biochip model.

Main Methods:

  • Development of a lung-on-chip fluidic macrodevice integrated with a pre-existing lung-on-membrane model (LOMM).
  • Culture of granulomas from blood samples of sarcoidosis patients and their introduction to the air-lung-interface of the microchip.
  • Measurement of cytokine levels (IL-1ß, IL-6, GM-CSF, INF-γ) after 48 hours using ELISA to compare responses between the LOMM with the 3D biochip pulmonary sarcoidosis model (3D BSGM) and the LOMM alone.

Main Results:

  • Statistically significant differences in the expression of key inflammatory cytokines, including IL-1ß, IL-6, and GM-CSF, were observed (P = 0.001953).
  • A trend towards significant difference was noted for INF-γ expression (P = 0.09375).
  • The study successfully established a functional 3D biochip model of pulmonary sarcoidosis.

Conclusions:

  • The developed 3D biochip pulmonary sarcoidosis model (3D BSGM) represents a novel platform for studying sarcoidosis in vitro.
  • This model, integrating microfluidics with patient-derived granulomas, offers a more physiologically relevant system for investigating sarcoidosis pathogenesis.
  • The observed cytokine differences highlight the model's utility in exploring the inflammatory mechanisms underlying sarcoidosis.