Publications by authors named "Hai-feng Ou Yang"

Article Synopsis
  • Researchers explored the use of Erythropoietin (EPO) gene-modified mesenchymal stem cells (MSCs) to combat airway remodeling in asthma, finding that these modified cells exhibited greater therapeutic effects compared to unmodified MSCs.
  • The study involved creating EPO-MSCs via a lentivirus vector, identifying their characteristics, and testing their impact on asthmatic mice through various analyses including histological evaluations and cytokine measurements.
  • Results indicated that EPO-MSCs significantly reduced airway inflammation, cell proliferation, and remodeling factors, potentially by inhibiting the TGF-β1-TAK1-p38MAPK signaling pathway.
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Article Synopsis
  • Chronic bronchial asthma leads to persistent airway inflammation and structural changes, making it hard to treat with existing drugs.
  • Interleukin-13 (IL-13) and IL-25 are key players in this inflammation and remodeling process.
  • Research showed that targeting both IL-13 and IL-25 at the same time reduced inflammation and tissue changes more effectively than treating with either one alone, suggesting a new potential treatment approach for asthma patients who don't respond well to current therapies.
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  • The study investigates KyoT2's role in asthma, focusing on airway remodeling and hyperresponsiveness.
  • KyoT2, which inhibits Notch signaling, was tested on asthmatic mice to assess its effects on airway structure and resistance.
  • Results showed that KyoT2 reduces Hes1 expression, lessens airway remodeling, and improves hyperresponsiveness, suggesting it could be a viable treatment for asthma.
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Subepithelial fibrosis is one of the common pathological features of asthmatic airway remodeling. During subepithelial fibrosis, type I collagen becomes the most abundant extracellular protein component. Studies have shown that Notch signaling participates in the progression of fibrosis; however, whether Notch signaling is involved in regulating type I collagen expression in airway fibroblasts remains unclear.

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Article Synopsis
  • The study investigates the effects of recombinant bacille Calmette-Guerin (rBCG) that expresses Der p2 on asthma, particularly its influence on Th17 cell differentiation and airway inflammation.
  • Results showed that transferring dendritic cells infected with Der p2 rBCG led to reduced airway inflammation and mucin production, effectively inhibiting excessive Th17 responses compared to traditional BCG.
  • The research highlights the importance of dendritic cells in rBCG's immunoregulatory functions and provides insight into the cellular mechanisms behind its potential as an asthma treatment.
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Article Synopsis
  • Notch signaling is shown to regulate the expression of MUC5AC, a key mucin in asthma-related mucus overproduction.
  • Various experiments revealed that activation of Notch can enhance MUC5AC promoter activity while Hes proteins can repress it.
  • This study suggests that targeting the Notch signaling pathway could provide new therapeutic options for managing mucus overproduction in asthma.
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Transfusion-related acute lung injury (TRALI) is a serious complication associated with blood transfusion and can cause transfusion associated fatalities. Both antibody dependent and non-dependent mechanisms are involved in TRALI, as proposed over the past years. Nonetheless, many details of the immune cells involved in TRALI, particularly the Mac1(+)/Gr1(+) cells from donors, are not fully understood yet.

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Article Synopsis
  • Researchers studied a recombinant bacille Calmette-Guérin (rBCG) vaccine expressing the Der p 2 allergen, which showed promise in reducing asthma symptoms by manipulating immune responses.
  • The study aimed to investigate the role of dendritic cells (DCs) in this process and involved transferring DCs from vaccinated mice to other mice to assess their impact on airway inflammation.
  • Results indicated that the transferred DCs significantly reduced asthmatic responses and promoted the development of regulatory T cells, suggesting that DCs are crucial for the rBCG's anti-asthma effects, especially through enhanced recruitment of certain DC subtypes.
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Article Synopsis
  • Mesenchymal stem cells (MSCs) show potential in reducing acute lung inflammation and fibrosis, but their effectiveness in allergic asthma is less understood.
  • MSCs were introduced into a mouse model of asthma, and their migration to inflamed lung tissues was tracked, revealing their movement depends on a specific chemical signal.
  • The study found that MSCs help mitigate allergic inflammation by promoting a shift from a T-helper 2 (Th2) to a T-helper 1 (Th1) immune response, suggesting MSC-based therapies could be beneficial for asthma treatment.
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  • The study investigates the role of bone marrow-derived adult stem cells in the airway remodeling process seen in asthma, which involves chronic inflammation and abnormal cell growth.
  • Using mice models, researchers established a chronic asthma condition and observed the presence of fluorescently labeled bone marrow cells in lung tissues.
  • The results indicate that a significant number of these cells contributed to the production of collagen and muscle in the lungs, suggesting they play a key role in asthma-related airway changes.
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Article Synopsis
  • Allergic asthma is driven by T helper (Th)2 cell immune responses, and new immunotherapy strategies aim to shift these responses towards Th1 to alleviate symptoms.
  • Previous studies demonstrated that a genetically modified form of bacille Calmette-Guerin (rBCG) could induce such a shift in naive mice, but its effectiveness in reducing allergic airway inflammation needed further investigation.
  • The current research showed that rBCG significantly reduced airway inflammation and related symptoms in allergic mice by promoting a Th1 response and enhancing regulatory T cells that suppress Th2 cells, indicating its potential as an effective asthma treatment.
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Evidence has shown that Notch signaling modulates CD4(+)CD25(+) regulatory T-cells (Tregs). As transcription factor Foxp3 acts as a master molecule governing the development and function of Tregs, we investigated whether Notch signaling might directly regulate Foxp3 expression. Here, we provide evidence that Notch signaling can modulate the FOXP3 promoter through RBP-J- and Hes1-dependent mechanisms.

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