CD101 eosinophil serves as an early response to suppress endotoxin-induced acute lung injury

Rationale: Acute lung injury (ALI) is characterized by respiratory distress, noncardiogenic pulmonary edema, abnormal coagulation, and pathologically extensive inflammation. Currently, accumulating researchers have focused on regulatory function of eosinophil in diseases. Intriguingly, a clinical investigation showed that the survived ALI patients displayed increased eosinophils in lung tissue. But the role and mechanism remains unclear. Based on the hypothesis, we observed the onset of inflammation, exaggerated inflammation burden and distant survival status using eosinophil-related ALI mice. Generally, our data implicated that eosinophil served as an early suppressor in acute lung injury. Methods: Eosinophil-related mouse strains are employed including eosinophil-deficient PHIL mice and IL-5 transgenic NJ1638 mice. Endobronchial LPS administration was conducted using PHIL mice, then neutrophils and eosinophils are analyzed by FACS and BALF. For eosinophil transfer, eosinophils are injected intratracheally 24 hours before LPS administration. Finally, surviving condition is reflected as body weight loss and 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. 3. Adaptive transfer of eosinophils to PHIL mice could release LPS induced 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.