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

Yoo Seob Shin, Jung Ho Sohn, Joo Young Kim, Jae Hyun Lee, Sang Heon Cho, Soo Jong Hong, Joo Shil Lee, Chein Soo Hong, Jungwon Park

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)593-602
Number of pages10
JournalYonsei medical journal
Volume53
Issue number3
DOIs
Publication statusPublished - 2012 May 1

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Cockroaches
Endotoxins
Inflammation
Goblet Cells
Hyperplasia
Intranasal Administration
Toll-Like Receptor 4
Interleukin-13
Allergens
Dimercaprol
Lymphocytosis
Respiratory Mucosa
Inbred C3H Mouse

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Shin, Yoo Seob ; Sohn, Jung Ho ; Kim, Joo Young ; Lee, Jae Hyun ; Cho, Sang Heon ; Hong, Soo Jong ; Lee, Joo Shil ; Hong, Chein Soo ; Park, Jungwon. / Endotoxin is not essential for the development of Cockroach induced allergic airway inflammation. In: Yonsei medical journal. 2012 ; Vol. 53, No. 3. pp. 593-602.
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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.",
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Shin, YS, Sohn, JH, Kim, JY, Lee, JH, Cho, SH, Hong, SJ, Lee, JS, Hong, CS & Park, J 2012, 'Endotoxin is not essential for the development of Cockroach induced allergic airway inflammation', Yonsei medical journal, vol. 53, no. 3, pp. 593-602. https://doi.org/10.3349/ymj.2012.53.3.593

Endotoxin is not essential for the development of Cockroach induced allergic airway inflammation. / Shin, Yoo Seob; Sohn, Jung Ho; Kim, Joo Young; Lee, Jae Hyun; Cho, Sang Heon; Hong, Soo Jong; Lee, Joo Shil; Hong, Chein Soo; Park, Jungwon.

In: Yonsei medical journal, Vol. 53, No. 3, 01.05.2012, p. 593-602.

Research output: Contribution to journalArticle

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T1 - Endotoxin is not essential for the development of Cockroach induced allergic airway inflammation

AU - Shin, Yoo Seob

AU - Sohn, Jung Ho

AU - Kim, Joo Young

AU - Lee, Jae Hyun

AU - Cho, Sang Heon

AU - Hong, Soo Jong

AU - Lee, Joo Shil

AU - Hong, Chein Soo

AU - Park, Jungwon

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N2 - 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.

AB - 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.

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