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Endotoxin is not essential for the development of cockroach induced allergic airway inflammation

Authors
 Yoo Seob Shin  ;  Jung-Ho Sohn  ;  Joo-Young Kim  ;  Jae Hyun Lee  ;  Sang-Heon Cho  ;  Soo-Jong Hong  ;  Joo-Shil Lee  ;  Chein-Soo Hong  ;  Jung-Won Park 
Citation
 YONSEI MEDICAL JOURNAL, Vol.53(3) : 593-602, 2012 
Journal Title
 YONSEI MEDICAL JOURNAL 
ISSN
 0513-5796 
Issue Date
2012
MeSH
Allergens/immunology* ; Animals ; Asthma/chemically induced* ; Asthma/immunology* ; Asthma/metabolism ; Cockroaches/immunology* ; Endotoxins/immunology* ; Enzyme-Linked Immunosorbent Assay ; Female ; Inflammation/chemically induced* ; Inflammation/immunology* ; Inflammation/metabolism ; Interferon-gamma/metabolism ; Interleukin-13/metabolism ; Interleukin-5/metabolism ; Mice ; Mice, Inbred BALB C ; Respiratory Hypersensitivity/chemically induced ; Respiratory Hypersensitivity/immunology*
Keywords
Cockroach ; endotoxin ; toll like receptor-4
Abstract
PURPOSE: Cockroach (CR) is an important inhalant allergen and can induce allergic asthma. However, the mechanism by which CR induces airway allergic inflammation and the role of endotoxin in CR extract are not clearly understood in regards to the development of airway inflammation. In this study, we evaluated whether endotoxin is essential to the development of CR induced airway allergic inflammation in mice. MATERIALS AND METHODS: Airway allergic inflammation was induced by intranasal administration of either CR extract, CR with additional endotoxin, or endotoxin depleted CR extract, respectively, in BALB/c wild type mice. CR induced inflammation was also evaluated with toll like receptor-4 (TLR-4) mutant (C3H/HeJ) and wild type (C3H/HeN) mice. RESULTS: Intranasal administration of CR extracts significantly induced airway hyperresponsiveness (AHR), eosinophilic and neutrophilic airway inflammation, as well as goblet cell hyperplasia in a dose-dependent manner. The addition of endotoxin along with CR allergen attenuated eosinophilic inflammation, interleukin (IL)-13 level, and goblet cell hyperplasia of respiratory epithelium; however, it did not affect the development of AHR. Endotoxin depletion in CR extract did not attenuate eosinophilic inflammation and lymphocytosis in BAL fluid, AHR and IL-13 expression in the lungs compared to CR alone. The attenuation of AHR, eosinophilic inflammation, and goblet cell hyperplasia induced by CR extract alone was not different between TLR-4 mutant and the wild type mice. In addition, heat inactivated CR extract administration induced attenuated AHR and eosinophilic inflammation. CONCLUSION: Endotoxin in CR extracts may not be essential to the development of airway inflammation.
Files in This Item:
T201201894.pdf Download
DOI
22477005
Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Park, Jung Won(박중원) ORCID logo https://orcid.org/0000-0003-0249-8749
Sohn, Jung Ho(손정호)
Shin, Yoo Seob(신유섭)
Lee, Jae Hyun(이재현) ORCID logo https://orcid.org/0000-0002-0760-0071
Hong, Chein Soo(홍천수)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/92098
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