title: Endotoxin is not essential for the development of cockroach induced allergic airway inflammation.
abstract: OBJECTIVE
  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.
  
  
  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.
  
  
  CONCLUSIONS
  Endotoxin in CR extracts may not be essential to the development of airway inflammation.
authors.affiliation: Department of Internal Medicine, Institute of Allergy, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Korea.
authors.forename: Yoo Seob
authors.initials: YS
authors.lastname: Shin
authors.forename: Jung-Ho
authors.initials: JH
authors.lastname: Sohn
authors.forename: Joo-Young
authors.initials: JY
authors.lastname: Kim
authors.forename: Jae Hyun
authors.initials: JH
authors.lastname: Lee
authors.forename: Sang-Heon
authors.initials: SH
authors.lastname: Cho
authors.forename: Soo-Jong
authors.initials: SJ
authors.lastname: Hong
authors.forename: Joo-Shil
authors.initials: JS
authors.lastname: Lee
authors.forename: Chein-Soo
authors.initials: CS
authors.lastname: Hong
authors.forename: Jung-Won
authors.initials: JW
authors.lastname: Park
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D001249:Asthma / Q000139:chemically induced* / Q000276:immunology* / Q000378:metabolism; D003058:Cockroaches / Q000276:immunology*; D004731:Endotoxins / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007249:Inflammation / Q000139:chemically induced* / Q000276:immunology* / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000276:immunology*
chemical_list: D000485:Allergens; D004731:Endotoxins; D018793:Interleukin-13; D015848:Interleukin-5; D007371:Interferon-gamma