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Background <p>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.</p> Aim <p>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. </p> Methods <p>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.</p> Results <p>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 response to LPS and HDM. Furthermore, we showed that inflammatory signaling alone, in the absence of direct LPS and HDM exposure, significantly reduces growth factor-induced adipogenesis and osteogenesis.</p> Conclusions <p>Taken together, our findings indicate that asthmatic inflammation not only reduces the number of lrMSCs but also impairs their function, potentially exacerbating disease progression by limiting their immunoregulatory role.</p>

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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)

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月22日

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  • Alicja Walewska,
  • Marlena Tynecka,
  • Sylwia Ksiezak,
  • Agnieszka Tarasik,
  • Adrian Janucik,
  • Kinga Bondarczuk,
  • Malgorzata Rusak,
  • Milena Dabrowska,
  • Hady Razak Hady,
  • Piotr Radziwon,
  • Dariusz Sredzinski,
  • Joanna Reszec-Gielazyn,
  • Marcin Moniuszko,
  • Andrzej Eljaszewicz

摘要

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 response to LPS and HDM. Furthermore, we showed that inflammatory signaling alone, in the absence of direct LPS and HDM exposure, significantly reduces growth factor-induced adipogenesis and osteogenesis.

Conclusions

Taken together, our findings indicate that asthmatic inflammation not only reduces the number of lrMSCs but also impairs their function, potentially exacerbating disease progression by limiting their immunoregulatory role.