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.
Papain-induced Acute Lung Injury Model
Acute lung injury is induced in C57BL/6 mice via intranasal administration of papain or PBS (control) daily for a period of 3 days, with the endpoint analysis at 7 days.
C57BL/6 mice were subjected to intranasal administration of papain for 3 days. After 7 days, immune cells in bronchoalveolar lavage fluid (BALF) were assessed. mCD45 positive cells (A) and eosinophils (B) in BALF samples were counted. The percentage of eosinophils in mCD45 was assessed (C). Values are expressed as mean ± SEM. One-way ANOVA with Bonferroni test, n=5, **P<0.01, ***P<0.001.
Histologic analysis of lungs via H&E and PAS (Periodic Acid Schiff) staining. Pathological changes were demonstrated by vascular and peribronchial mixed inflammatory cell infiltration (top) and excess mucus formation in some bronchi as visualized by PAS staining. Scoring of inflammatory cell infiltration and bronchial mucus around blood vessels and bronchi of papain-induced asthma model in C57BL/6 mice indicates a significant increase compared to control tissues. Values are expressed as mean ± SEM. *** p<0.001, **p<0.01, *p<0.05.
Alternaria-induced Acute Lung Injury Model
Acute lung injury is induced in C57BL/6 mice via intranasal administration of ALT (100μg/80μL) or PBS (Control) daily for a period of 4 days.
Assessment of the number and percentage of eosinophils in the mCD45+ population indicates an increased presence of eosinophils in the BALF of the alternaria-induced acute lung injury mouse model. Values are expressed as mean ± SEM. **** p<0.0001, **p<0.01.