IL-1β Blocker and Its Influence on Preserving Lung Tissues Sensitized by Echinococcus granulosus Sac Fluid by
Chun-Sheng Wang1, Xilizhati Kulaixi1, Jing-Ru Zhou1
1Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830000, Xinjiang, China.
Introduction:
This study aimed to elucidate the molecular mechanisms underlying macrophage involvement in lung injury following sensitization to the cyst fluid induced by Echinococcus granulosus.
Methods:
Eighteen C57/BL6 mice were randomly divided into three groups, with six mice in each group. After mice were intraperitoneally injected with Echinococcus granulosus, they were raised for 3 months. In the control group (group A, n = 6), normal saline was injected into the abdominal cavity and airway. In the blocker group (group B, n=6), IL-1β blocker was injected through the tail vein, followed by intraperitoneal injection of 0.1 ml/g Echinococcus granulosus cyst fluid and airway injection of 0.05 ml/g Echinococcus granulosus cyst fluid. In the sensitized group (group C, n = 6), 0.1 ml/g Echinococcus granulosus cyst fluid was injected intraperitoneally, and 0.05 ml/g Echinococcus granulosus cyst fluid was injected into the airway. Changes in macrophages in lung tissue were detected by flow cytometry. The pathological sections of lung tissue were prepared, and immunohistochemical analysis was performed. At the same time, the lung tissues of the three groups of mice were analyzed by Western blot and RT-PCR. The protein and mRNA expression of PI3K/AKT/NF-κB and the levels of inflammatory factors IL-6 and TNF-α were detected.
Results:
After the application of IL-1β blockers, the number of M2-type macrophages in the lungs increased significantly, the mRNA and protein expression levels of PI3K/AKT/ NF-κB and inflammatory factors IL-6 and TNF-α decreased, and the damage was significantly alleviated.
Discussion:
The findings suggest that IL-1β drives lung injury in E. granulosus sensitization by skewing macrophages toward a pro-inflammatory phenotype and activating the PI3K/AKT/NF-κB pathway. The protective effect of IL-1β blockade highlights its potential as a therapeutic target to modulate macrophage polarization and mitigate inflammation in hydatid disease-related lung injury.
Conclusion:
IL-1β blockers exert a protective effect on lung injury caused by allergic reactions to the cystic fluid of Echinococcus granulosus by promoting an increase in the M2 phenotype of macrophages.
