Abstract
dc:descriptionPURPOSE: Cockroach (CR) is an important inhalant allergen and can make a mouse asthma model. However, mechanism underlying the CR-induced mouse model of asthma is not clear and the role of endotoxin contaminated in CR allergen remains controversial. Therefore, we evaluated the role of endotoxin and toll like receptor-4 (TLR-4) for the induction of asthma in mouse model. METHODS: CR allergen was delivered intranasally to BALB/C mouse, TLR-4 mutant (C3H/HeJ) or wild type (C3H/HeN) mouse without any adjuvant. Asthma was induced by CR, CR with endotoxin added (10,000 EU/mouse) or endotoxin-depleted CR, respectively. RESULTS: CR asthma model can be produced by intranasal sensitization of CR allergen, dose dependently. CR can induce airway hyper-responsiveness (AHR) to methacholine, eosinophilic and neutrophilic inflammation, and airway mucus gland hyperplasia. Endotoxin added in CR attenuated eosinophilic inflammation, IL-13 in BAL fluid, and goblet cell hyperplasia of respiratory epithelium, however, did not affect AHR. Endotoxin-depleted CR also attenuated eosinophilic inflammation and lymphocytosis in BAL fluid, but did not affect AHR and IL-13 levels in BAL fluid compared to CR group. AHR, eosinophilic inflammation, and goblet cell hyperplasia induced by CR were more exacerbated in TLR-4 mouse than in wild type mouse. CONCLUSION: CR can induce allergic asthma model presenting increased AHR, eosinophilic and neutrophilic inflammation, and goblet cell hyperplasia. However, endotoxin in the CR dose not appears to affect the development of AHR, eosinophilic inflammation, and epithelial goblet cell hyperplasia in CR-induced mouse model of asthma.
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
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- 신, 유섭
- Contributors dc:contributor
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- 박, 해심
- 대학원 의학과
- 103243
Subjects
dc:subject × 3Rights
- Language dc:language
- en
Identifiers
dc:identifier.*- Identifier
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http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000009182
000000009182 - OAI identifier oai:identifier
- oai:repository.ajou.ac.kr:201003/1437