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Updated: Jun 9, 2025
Author Spotlight: Developing a Microfluidic Lung-on-Chip Model for In-Depth Study of Human Immune Response and Infection Mechanisms
Published on: May 31, 2024
Monitoring the Cascade of Monocyte-Derived Macrophages to Influenza Virus Infection in Human Alveolus Chips
Chenguang Wang1, Shujun Liu1, Chuyu Li1
1School of Medical Technology, Beijing Institute of Technology, Beijing 100081, P. R. China.
Abstract:
Respiratory viruses ravage the world and seriously threaten people's health. Despite intense research efforts, the immune mechanism underlying respiratory virus-induced acute lung injury (ALI) and pulmonary fibrosis (PF) has not been fully elucidated. Here, the cascade of monocyte-derived macrophages to influenza A virus infection is monitored on an optimized human alveolus chip to reveal the role of macrophages in the development of ALI and PF. We find that viral infection causes damage to the alveolar air-liquid barrier and the release of inflammatory cytokines, which induce the M0 macrophages to gather and polarize to the M1 phenotype at the damaged site through recruitment, adhesion, migration, and activation, leading to ALI. Afterward, M1 macrophages polarize into the M2 phenotype, and then transform into myofibroblasts, followed by enhanced secretion of various anti-inflammatory cytokines and profibrotic cytokines, to promote PF. Our study provides an insight into the pathogenesis of virus-induced ALI and PF, which will assist in the development of therapeutic strategies and drugs for treating influenza and other respiratory virus infections.
Insights
Macrophages play a key role in virus-induced lung injury. They initially cause acute lung injury (ALI) and then promote pulmonary fibrosis (PF) by changing their function and form.
Area of Science:
- Immunology
- Pathology
- Virology
Background:
- Respiratory viruses cause significant global health issues.
- The immune mechanisms behind virus-induced acute lung injury (ALI) and pulmonary fibrosis (PF) remain unclear.
- Macrophages are crucial immune cells involved in lung inflammation and repair.
Purpose of the Study:
- To elucidate the role of macrophages in the pathogenesis of ALI and PF following influenza A virus infection.
- To monitor macrophage behavior in response to viral infection using a human alveolus chip model.
Main Methods:
- Utilized an optimized human alveolus chip to simulate viral infection.
- Monitored the dynamic cascade of monocyte-derived macrophages (M0) during influenza A virus infection.
- Analyzed macrophage polarization (M1 and M2 phenotypes) and transformation into myofibroblasts.
Main Results:
- Viral infection damaged the alveolar air-liquid barrier, releasing inflammatory cytokines.
- M0 macrophages were recruited, adhered, migrated, and activated, polarizing to the M1 phenotype, causing ALI.
- M1 macrophages subsequently polarized to the M2 phenotype and transformed into myofibroblasts, secreting cytokines that promoted PF.
Conclusions:
- Macrophages orchestrate the progression from ALI to PF after viral infection.
- Understanding this macrophage-driven cascade offers insights into treating virus-induced lung diseases.
- This study aids in developing targeted therapeutic strategies for influenza and other respiratory viral infections.
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