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<p>Blast lung injury (BLI) is characterized by pulmonary inflammatory response and tissue injury. A rat BLI model was established using a biomedical shock tube, and the animals were divided into three groups: control, BLI model, and IL-17&#xa0;A inhibitor groups. We assessed pulmonary function parameters, observed lung hemorrhage and pleural effusion, measured white cell counts in bronchoalveolar lavage fluid (BALF), quantified histopathological scores using hematoxylin and eosin (HE) staining, and analyzed the protein expression levels of IL-17&#xa0;A, phospho-NF-κB p65, and inhibitor of κB kinase β (IKK-β) by Western blotting. Compared with the control group, the model group exhibited significantly increased respiratory frequency and airway resistance index. In contrast, the IL-17&#xa0;A inhibitor group demonstrated significantly improved minute ventilation and peak inspiratory and expiratory flow rates. The inhibitor group also demonstrated reduced pulmonary hemorrhage and pleural effusion, lower BALF white cell counts, and reduced histopathological scores. Western blot analysis revealed that the expression levels of IL-17&#xa0;A, p-p65, and IKK-β were upregulated in the model group, but were robustly suppressed by IL-17&#xa0;A inhibition. In conclusion, IL-17&#xa0;A inhibition effectively attenuated blast-induced pulmonary inflammatory injury, improved pulmonary function, and mitigated histopathological injury, potentially through modulation of the IL-17&#xa0;A/NF-κB signaling pathway.</p>

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IL-17 A inhibition attenuates pulmonary inflammation following blast lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月24日

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  • Hong Wang,
  • Yuhao Zhang,
  • Xiaolin Fan,
  • Liang Li,
  • Ning Ma,
  • Boya Yu,
  • Xiao Li,
  • Qing Lu,
  • Junhong Gao

摘要

Blast lung injury (BLI) is characterized by pulmonary inflammatory response and tissue injury. A rat BLI model was established using a biomedical shock tube, and the animals were divided into three groups: control, BLI model, and IL-17 A inhibitor groups. We assessed pulmonary function parameters, observed lung hemorrhage and pleural effusion, measured white cell counts in bronchoalveolar lavage fluid (BALF), quantified histopathological scores using hematoxylin and eosin (HE) staining, and analyzed the protein expression levels of IL-17 A, phospho-NF-κB p65, and inhibitor of κB kinase β (IKK-β) by Western blotting. Compared with the control group, the model group exhibited significantly increased respiratory frequency and airway resistance index. In contrast, the IL-17 A inhibitor group demonstrated significantly improved minute ventilation and peak inspiratory and expiratory flow rates. The inhibitor group also demonstrated reduced pulmonary hemorrhage and pleural effusion, lower BALF white cell counts, and reduced histopathological scores. Western blot analysis revealed that the expression levels of IL-17 A, p-p65, and IKK-β were upregulated in the model group, but were robustly suppressed by IL-17 A inhibition. In conclusion, IL-17 A inhibition effectively attenuated blast-induced pulmonary inflammatory injury, improved pulmonary function, and mitigated histopathological injury, potentially through modulation of the IL-17 A/NF-κB signaling pathway.