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Updated: Jun 29, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
[Experimental study on role of endotoxin in induction of murine model of allergic asthma]
Xiaoyu Zhou1, Wei Shi, Qian Zhang
1School of Public Health, Fudan University, Shanghai 200032, China. 032102076@fudan.edu.cn
Objective:
To study the effect of lipopolysaccharide (LPS) on allergen sensitization and challenge in allergic asthma model of mice based on a murine model of allergic asthma.
Methods:
BALB/c mice were separated into four experimental groups and two control groups. Those were allergen (OVA) sensitization and challenge one, OVA sensitization and exposure to LPS one, OVA sensitization and exposure to LPS during OVA challenge one, and exposure to LPS during OVA sensitization and OVA challenge one. There were also reagent group and healthy one as control. Each experimental group was treated with three doses of LPS. Lung functional disorder was demonstrated by assessing resistance of airway and pulmonary compliance. Expression of CD4+ CD25+ regulatory T cells (Treg cells) was measured by flow cytometry (FCM). Expressions of transcription factor, Foxp3 mRNA, which was extracted from lung and spleen issues, were assayed by real-time quantitative polymerase chain reaction (real-time PCR). Total and OVA-specific IgE levels in blood plasma were quantified by ELISA assay. Inflammation was assessed by determining total and differential leukocyte counts and T-helper type 2 cytokine (IL-4 and IL-5) levels in bronchoaleolar lavage fluid (BALF). Lung tissues were sliced and stained to observe the changes of histology by light microscope.
Results:
The results showed that LPS might shift cytokine response toward a Th1 response and away from a Th2 response, might reduce the level of plasma IgE and induce proliferation of Treg cells, thereby confer benefits on lung function of experimental animals. More significant immunoprotection roles in the groups treated with LPS were found through peritoneal injection before allergen sensitization. Less severe inflammatory response, less lung function injury and higher expression of Foxp3 were noticed in the group.
Conclusion:
It was suggested that endotoxin might restrain Th2 response and might be related to the expression increase of Foxp3, hence subsequently might alleviate asthmatic symptoms.
