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A2256 - Eosinophil Protects Against the Onset of Inflammation in Acute Lung Injury
Author Block: C. Zhu1, L. Zhou1, Y. Zhao1, F. Li1, Y. Wu1, Y. Wu1, Z. Li1, M. Li1, Q. Weng1, Y. Hu1, C. Zhang1, S. Ying2, Z. Chen1, H. Shen1, W. Li1; 1Zhejiang University, Hangzhou, China, 2Department of Pharmacology, Zhejiang University, Hangzhou, China.
Rationale. Acute lung injury (ALI) is a fatal clinical condition characterized by respiratory distress, noncardiogenic pulmonary edema, abnormal coagulation, and pathologically extensive inflammation. Currently, accumulating investigations have focused on immunoregulatory function of eosinophil in pulmonary hemostasis, and very interestingly, a clinical exploration demonstrated that the presence of eosinophil in lungs reveal lower mortality in ALI patients, but the role and function of eosinophil in ALI still remains blurred. Based on the hypothesis, we uncover that eosinophil depletion result in accelerated onset of inflammation, exaggerated inflammation burden and distant survival status in ALI mice. Likewise, eosinophil adaptive transfer could restrain neutrophil concentration and improve living condition. Generally, our data implicated that eosinophil served as a protective role in ALI.
Methods. Eosinophil-related mouse strains are employed in this project include eosinophil-deficient PHIL mice and IL-5 transgenic NJ1638 mice. And both strains are generous gifts from Prof. James Lee. Firstly, we offer PHIL mice and wildtype mice endobronchial LPS administration, and then detect neutrophils and eosinophils using FACS. Classified counts of cells in bronchialveolar lavage fluid are also conducted to validate the results above. For eosinophil transfer, eosinophils are purified from peripheral blood of NJ1638 mice, each ALI mice are injected intratracheally 24 hours before LPS administration. Finally, surviving condition is reflected as the calculation of body weight loss and portraying of surviving curve.
Results. 1. A transient eosinophil alternation is detected in wildtype mice post LPS injection during the onset of inflammation. 2. PHIL mice display elevated neutrophilic recruitment in very acute phase compared to wildtype mice. 3. Adaptive transfer of eosinophils to PHIL mice could release LPS induced exaggerated inflammation. 4. PHIL mice who received LPS inoculation suffer harsher body weight loss and inferior odds of survival.
Conclusion. Eosinophil is a protective aspect in acute lung injury; therefore loss of eosinophil might lead to exacerbated inflammation and worse living status.