Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness

Kirstein, F, Horsnell, W, Nieuwenhuizen, N, Ryffel, B, Lopata, A and Brombacher, F 2010, 'Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness', Infection and Immunity, vol. 78, no. 9, pp. 4077-4086.


Document type: Journal Article
Collection: Journal Articles

Title Anisakis pegreffii-Induced Airway Hyperresponsiveness Is Mediated by Gamma Interferon in the Absence of Interleukin-4 Receptor Alpha Responsiveness
Author(s) Kirstein, F
Horsnell, W
Nieuwenhuizen, N
Ryffel, B
Lopata, A
Brombacher, F
Year 2010
Journal name Infection and Immunity
Volume number 78
Issue number 9
Start page 4077
End page 4086
Total pages 10
Publisher Amer Soc Microbiology
Abstract Infection with the fish parasite Anisakis following exposure to contaminated fish can lead to allergic reactions in humans. The present study examined the immunological mechanisms underlying the development of allergic airway inflammation in mice after different routes of sensitization to Anisakis. Wild-type and interleukin-4 receptor alpha (IL-4R)-deficient BALB/c mice were sensitized intraperitoneally with live or heat-killed Anisakis larvae or by intranasal administration of an Anisakis extract and were subsequently challenged intranasally with an Anisakis extract. Both routes of sensitization induced IL-4R-dependent allergic airway responses, whereas allergen-specific antibody responses developed only when mice were sensitized intraperitoneally. Intranasal sensitization induced airway hyperresponsiveness (AHR) in wild-type mice only, showing that AHR was IL-4/IL-13 dependent. Unexpectedly, infection with Anisakis larvae induced AHR in both wild-type and IL-4R-deficient mice. IL-4R-independent AHR was mediated by gamma interferon (IFN-), as evidenced by the fact that in vivo neutralization of IFN- abrogated AHR. Together, these results demonstrate that both infection with larvae and inhalational exposure to Anisakis proteins are potent routes of allergic sensitization to Anisakis, explaining food- and work-related allergies in humans. Importantly for diagnosis, allergic airway inflammation can be independent of detectable Anisakis-specific antibodies. Moreover, depending on the route of sensitization, AHR can be induced either by IL-4/IL-13 or by IFN-.
Subject Biological Sciences not elsewhere classified
Keyword(s) Protein Contact-Dermatitis
Eosinophilic Inflammation
Allergic-Asthma
Deficient Mice
Mouse Model
Ifn-Gamma
Simplex
Hyperreactivity
Il-13
Fish
DOI - identifier 10.1128/IAI.01131-09
Copyright notice Copyright © 2010, American Society for Microbiology. All Rights Reserved.
ISSN 0019-9567
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