67 88

Cited 0 times in

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

Authors
 Yoo Seob Shin  ;  Jung-Ho Sohn  ;  Jung-Won Park  ;  Chein-Soo Hong  ;  Joo-Shil Lee  ;  Soo-Jong Hong  ;  Sang-Heon Cho  ;  Jae Hyun Lee  ;  Joo-Young Kim 
Citation
 Yonsei Medical Journal, Vol.53(3) : 593-602, 2012 
Journal Title
 Yonsei Medical Journal 
ISSN
 0513-5796 
Issue Date
2012
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.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/92098
DOI
10.3349/ymj.2012.53.3.593
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실)
Yonsei Authors
박중원(Park, Jung Won) ; 손정호(Sohn, Jung Ho) ; 신유섭(Shin, Yoo Seob) ; 이재현(Lee, Jae Hyun) ; 홍천수(Hong, Chein Soo)
사서에게 알리기
  feedback
Files in This Item:
T201201894.pdf Download
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse