The influence of asthmatic inflammation and house dust mite (HDM) exposure on abundance, immune-modulatory potential, and differentiation capacity of the lung-resident mesenchymal stem cells (lrMSCs).
Walewska A., Tynecka M., Ksiezak S., Tarasik A., Janucik A., Bondarczuk K.
Animal Study on Immune Modulation, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Animal Study
- Journal
- Stem Cell Res Ther (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40696474
- PMCID
- PMC12281997
- DOI
- 10.1186/s13287-025-04520-1
Abstract (original English)
Background Tissue-resident mesenchymal stem cells, also known as mesenchymal stromal cells (MSCs), play a crucial role in maintaining tissue homeostasis and repair. However, their function in chronic inflammatory diseases, such as asthma, remains elusive. Aim Here, we aimed to assess the influence of house dust mite (HDM)-induced asthmatic inflammation on the numbers and function of lung resident (lr)MSCs. Methods Experimental asthma was induced in female C57BL6/cmdb mice via intranasal HDM administration. LrMSCs were isolated, expanded, and characterized by flow cytometry and differentiation assays. Human adipose tissue-derived (hAD)MSCs were isolated and stimulated with HDM, LPS, or cytokines. Co-culture experiments with peripheral blood mononuclear cells (PBMCs) assessed immunomodulatory potential. Gene expression, cytokine levels, and T-cell proliferation were analyzed. Results Here, we showed that asthmatic lung inflammation significantly reduces the number of lrMSCs. More importantly, remaining lrMSCs showed impaired differentiation potential and lacked immunomodulatory functions. Furthermore, we found that exposure of hAD-MSCs to HDM and LPS similarly led to marked inhibition of differentiation potential and suppression of immunosuppressive activities. Notably, this inhibitory effect persisted despite the presence of pro-inflammatory cytokines released by PBMCs in respon
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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