The acute lung injury (ALI) mouse model is employed to investigate the mechanisms of acute lung injury and therapeutic interventions.
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Acute lung inflammation can be incited in response to a variety of allergens, chemicals, or pathogens. Alternaria and papain are allergens that can disrupt the airway epithelium, triggering a rapid eosinophilic inflammation mediated by innate lymphoid cell activation. Intranasal administration of alternaria or papain can be used to recapitulate acute lung injury/inflammation in mice.
The acute lung injury (ALI) mouse model is employed to investigate the mechanisms of acute lung injury and therapeutic interventions. This model is generally induced by administering cytokines, chemical agents (such as lipopolysaccharide, LPS), or physical stimuli to evoke acute lung inflammation. It leads to pathological changes such as pulmonary edema, inflammatory cell infiltration, and impaired gas exchange. Researchers focus on the inflammatory processes in the lungs to explore potential treatment strategies and improve patient outcomes.
| Readout | ||
| Included tests | Bronchoalveolar Lavage Fluid (BALF) | Cell numbers of Neutrophils, eosinophils, and macrophages |
| Histopathology | Bronchial mucus | |
| Optional tests | BALF | IL-4, IL-5, IL-13, TARC… |
| Lung tissue homogenate | IL-4, IL-5, IL-13, TARC… | |
The count of mCD45 and Eosinophils as well as Percentage of eosinophils in mCD45. The score of Inflammatory cell infiltration and bronchial mucus around blood vessels and bronchi of papain-induced acute lung injury mouse model based on C57BL/6 mice. Values are expressed as mean ± SEM. *** p<0.001, **p<0.01, *p<0.05.
In C57BL/6N mice, the PBS control group (G1) showed no significant abnormalities under the microscope. Compared to the control group (G1), the three dosage groups of the papain model (G2-35ug/40uL, G3-50ug/40uL, and G4-75ug/40uL) exhibited varying degrees of vascular and peribronchial inflammatory cell infiltration, mucus in the lung bronchi, and eosinophil infiltration around the lung blood vessels and bronchi, indicating successful modeling. There was no significant difference in the degree of modeling among the three dosage groups.
| Readout | ||
| Included tests | Bronchoalveolar Lavage Fluid (BALF) | Cell numbers of Neutrophils, eosinophils, and macrophages |
| Histopathology | Bronchial mucus | |
| Optional tests | BALF | IL-4, IL-5, IL-13, TARC… |
| Lung tissue homogenate | IL-4, IL-5, IL-13, TARC… | |
Eosinophils and percentage of eosinophils in mCD45 were elevated in BALF of acute lung injury mouse model. Values are expressed as mean ± SEM. **** p<0.0001, **p<0.01.
| Readout | ||
| Included tests | Bronchoalveolar Lavage Fluid (BALF) | Cell numbers of Neutrophils, eosinophils, and macrophages |
| Serum | IgE level | |
| Histopathology | Bronchial mucus | |
| Immune infiltration | ||
| Histology scores | ||
| Optional tests | BALF | Total IgE, IL-4, IL-5, IL-13, TARC… |
| Lung tissue homogenate | IL-4, IL-5, IL-13, TARC… | |
| Lung tissue | IHC | |
| Airway function testing | Enhanced Pause (Penh) | |
The asthma model was induced in B-hTSLP/hTSLPR mice using TSLP/OVA. (A) The number of CD45+ cells in BALF. (B) The number of eosinophils in BALF. (C) The proportion of eosinophils to CD45 + cells. The results showed that after sensitization and challenge with OVA/IL33, the leukocyte infiltration of mice in G2-G3 model group was significantly increased compared with G1 control group, and their eosinophil content was significantly increased, suggesting that the model was successfully established. (D) Serum was isolated at the day7、day14 of the experiment and concentrations of mouse Total IgE were measured using ELISA.
H&E staining in the lungs of asthmatic mice. In contrast to the G1 untreated group, the TSLP/OVA-treated G2 model animals showed asthma-related pathological changes as demonstrated by vascular and peribronchial mixed inflammatory cell infiltration(E) and mucus (F) formation in some bronchi.
