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Circulating SSEA-1+ stem cell-mediated tissue repair in allergic airway inflammation
Chiao-Juno Chiu1, Chien-Chia Liao2, Yu-Hsiang Hsu3
1Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Insights
In asthma, lung stem cells decrease, but circulating stem cells increase and migrate to the lungs. These cells repair lung damage and reduce inflammation, offering a potential therapeutic strategy.
Area of Science:
- Pulmonary Medicine
- Stem Cell Biology
- Immunology
Background:
- Chronic/severe asthma is characterized by airway remodeling and lung dysfunction.
- Neonatal SSEA-1+ pulmonary stem/progenitor cells (PSCs) previously showed potential in ameliorating airway inflammation in asthmatic mice.
- The precise mechanisms of endogenous adult lung SSEA-1+ PSCs in maintaining alveolar homeostasis and lung repair after allergen challenge are not fully understood.
Purpose of the Study:
- To investigate the expression profile of endogenous adult lung SSEA-1+ cells in asthmatic mice.
- To clarify the biological significance and therapeutic potential of these cells in allergic asthma models.
- To elucidate the molecular mechanisms underlying their protective effects.
Main Methods:
- Confocal microscopy and cytometric analysis were used to determine lung and circulating SSEA-1+ cells.
- GFP chimeric mice facilitated in vivo cell lineage tracing.
- Adoptive transfer of circulating SSEA-1+ cells was performed in ovalbumin- and house dust mite-induced allergic asthma models.
Main Results:
- Endogenous lung SSEA-1+ cells were significantly reduced in asthmatic mice, while circulating SSEA-1+ cells were enriched post-challenge.
- Adoptively transferred circulating SSEA-1+ cells exhibited lung-specific homing via the CXCR7-CXCL11 axis.
- These cells reduced inflammatory cell infiltration, goblet cell hyperplasia, smooth muscle thickening, and mucus production, thereby ameliorating lung inflammation and structural damage.
Conclusions:
- Circulating SSEA-1+ cells represent a unique population that migrates to the lung in response to allergen challenge.
- These cells possess transdifferentiation capacity and exert protective effects by mitigating inflammation and structural damage.
- Enhancing the bone marrow-derived circulating SSEA-1+ cell pool in the lung offers a potential rescue mechanism for maintaining alveolar homeostasis and promoting tissue repair in asthma.
Abstract:
Structural changes known as airway remodeling characterize chronic/severe asthma and contribute to lung dysfunction. We previously reported that neonatal SSEA-1+ pulmonary stem/progenitor cells (PSCs) ameliorated airway inflammation in asthmatic mice. However, the molecular mechanisms by which endogenous SSEA-1+ PSC of adult mice afford beneficial effects in alveolar homeostasis and lung repair after allergen challenge remain incompletely understood. To analyze the expression profile and clarify the biological significance of endogenous adult lung SSEA-1+ cells in asthmatic mice. Lung SSEA-1+ cells and circulating SSEA-1+ cells in peripheral blood were determined by confocal microscopy and cytometric analysis. GFP chimeric mice were used to trace cell lineage in vivo. The roles of circulating SSEA-1+ cells were verified in ovalbumin-induced and house dust mite-induced allergic asthmatic models. In asthmatic mice, endogenous lung SSEA-1+ cells almost disappeared; however, a unique population of circulating SSEA-1+ cells was enriched after the challenge phase. In asthmatic mice, adoptive transfer of circulating SSEA-1+ cells had a specific homing preference for the lung in response to inhaled antigen through upregulating CXCR7-CXCL11 chemokine axis. Circulating SSEA-1+ cells can transdifferentiate in the alveolar space and ameliorate lung inflammation and structural damage through inhibiting the infiltration of inflammatory cells into peribronchovascular and goblet cell hyperplasia areas, reducing the thickened smooth muscle layers and PAS-positive mucus-containing goblet cells. Reinforcing bone marrow-derived circulating SSEA-1+ cells from peripheral blood into lung tissue which create a rescue mechanism in maintaining alveolar homeostasis and tissue repair to mediate lung protection for emergency responses after allergen challenge in asthmatic conditions.
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