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<p>Stem cells from human exfoliated deciduous teeth (SHEDs) are self-renewing mesenchymal stem cells residing within the perivascular niche of the dental pulp. Previous studies have shown that SHEDs can attenuate acute lung injury and fibrosis. The effects of SEHDs on airway inflammation and airway hyperresponsiveness (AHR) were investigated in a mouse model of allergic asthma. In addition, clinical characteristics expected to respond well to SHED treatment were identified in co-culture experiments of peripheral blood mononuclear cells (PBMCs) and SHEDs from asthma patients. SHED treatment significantly decreased AHR, inflammatory cell counts in bronchoalveolar lavage fluid, and Th2 cytokine levels. In co-culture experiments using the patient’s PBMCs and SHEDs, the levels of interleukin (IL)-4 in cultures from ex-smoker asthma patients decreased significantly, and the IL-4 level was shown to correlate with the patient’s smoking history (pack-years). In mouse, SHED treatment decreased airway inflammation and AHR. In asthmatic patients with a history of smoking, IL-4 levels are significantly higher such that SHED treatment will be of particular benefit to this population. Nevertheless, given the small sample size and the absence of long-term follow-up, the findings should be interpreted with caution. Additional well-designed studies are warranted to validate these results.</p>

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Effects of mesenchymal stem cells derived from human exfoliated deciduous teeth (SHEDs) on airway inflammation in a murine model of acute asthma

  • 期刊论文

  • 发表日期：

    2025年10月1日

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  • Shin Young Kim,
  • Hyoung Kyu Yoon,
  • Tai Joon An,
  • Seo Hyun Kim,
  • Yong Suk Jo,
  • Joon Young Choi,
  • Jung Hur,
  • Chin Kook Rhee

摘要

Stem cells from human exfoliated deciduous teeth (SHEDs) are self-renewing mesenchymal stem cells residing within the perivascular niche of the dental pulp. Previous studies have shown that SHEDs can attenuate acute lung injury and fibrosis. The effects of SEHDs on airway inflammation and airway hyperresponsiveness (AHR) were investigated in a mouse model of allergic asthma. In addition, clinical characteristics expected to respond well to SHED treatment were identified in co-culture experiments of peripheral blood mononuclear cells (PBMCs) and SHEDs from asthma patients. SHED treatment significantly decreased AHR, inflammatory cell counts in bronchoalveolar lavage fluid, and Th2 cytokine levels. In co-culture experiments using the patient’s PBMCs and SHEDs, the levels of interleukin (IL)-4 in cultures from ex-smoker asthma patients decreased significantly, and the IL-4 level was shown to correlate with the patient’s smoking history (pack-years). In mouse, SHED treatment decreased airway inflammation and AHR. In asthmatic patients with a history of smoking, IL-4 levels are significantly higher such that SHED treatment will be of particular benefit to this population. Nevertheless, given the small sample size and the absence of long-term follow-up, the findings should be interpreted with caution. Additional well-designed studies are warranted to validate these results.