AI Article Synopsis
- The study examined how B lymphocytes influence the balance between Th1 and Th2 immune responses in pulmonary fibrosis caused by hypersensitivity pneumonia in rats.
- Using different rat models, they found that the involvement of B cells and the Notch signaling pathway was crucial for developing this condition, as indicated by various staining and protein analysis methods.
- Specifically, eliminating B cells or inhibiting the Notch pathway successfully corrected the Th1/Th2 imbalance and reduced the severity of pulmonary fibrosis.
Article Abstract
Introduction: We investigated the molecular mechanism by which B lymphocytes regulate Th1/Th2 imbalance to participate in the pulmonary fibrosis in hypersensitivity pneumonia induced by pigeon shedding in rats.
Methods: CD19+ rats and CD19- rats were used to construct animal models of fibrotic hypersensitivity pneumonia. DAPT was used to inhibit the Notch signaling pathway. The pathological changes were assessed with HE and Masson staining. Protein level was detected with Western blot. Th1/Th2 ratio was analyzed with flow cytometry. Cytokine levels were measured with ELISA.
Results: The pathological changes of pulmonary fibrosis were not obvious in the CD19- rats and after DAPT treatment. Notch signaling pathway proteins, including Notch1, Notch2, Jag1, Jag2, DLL1, and DLL4, in lung tissues of model rats were all significantly upregulated than those in control rats. However, these proteins in CD19- rats were lower in CD19+ rats, suggesting that B cells play a key role in inducing pneumonia. Besides, the Th1/Th2 ratio in the BALF of model rats decreased, which was further reversed by DAPT. However, we found that in CD19- rats, the regulation of the Th1/Th2 ratio by the Notch signaling pathway was lost.
Conclusion: Deleting B lymphocytes or blocking the Notch pathway both reversed the Th1/Th2 imbalance in fibrotic hypersensitivity pneumonia and inhibited pulmonary fibrosis.
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| http://dx.doi.org/10.1159/000527533 | DOI Listing |
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