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

Kirstein, Frank; Horsnell, William G. C.; Nieuwenhuizen, Natalie E.; Ryffel, Bernhard; Lopata, Andreas L.; Brombacher, Frank

doi:10.1128/iai.01131-09

Cited by 19 publications

(14 citation statements)

References 44 publications

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“…Others have demonstrated that inhibiting the IL-4R-STAT6 pathway may not be sufficient to inhibit alternative pathways capable of promoting AHR [31,78]. In a chronic inhalation model, airway inflammation and AHR in STAT6-/- mice coincided with a switch to a Th1 response [79].…”

Section: Discussionmentioning

confidence: 99%

The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

et al. 2013

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Severe, glucocorticoid-resistant asthma comprises 5-7% of patients with asthma. IL-17 is a biomarker of severe asthma, and the adoptive transfer of Th17 cells in mice is sufficient to induce glucocorticoid-resistant allergic airway disease. Nitrogen dioxide (NO2) is an environmental toxin that correlates with asthma severity, exacerbation, and risk of adverse outcomes. Mice that are allergically sensitized to the antigen ovalbumin by exposure to NO2 exhibit a mixed Th2/Th17 adaptive immune response and eosinophil and neutrophil recruitment to the airway following antigen challenge, a phenotype reminiscent of severe clinical asthma. Because IL-1 receptor (IL-1R) signaling is critical in the generation of the Th17 response in vivo, we hypothesized that the IL-1R/Th17 axis contributes to pulmonary inflammation and airway hyperresponsiveness (AHR) in NO2-promoted allergic airway disease and manifests in glucocorticoid-resistant cytokine production. IL-17A neutralization at the time of antigen challenge or genetic deficiency in IL-1R resulted in decreased neutrophil recruitment to the airway following antigen challenge but did not protect against the development of AHR. Instead, IL-1R-/- mice developed exacerbated AHR compared to WT mice. Lung cells from NO2-allergically inflamed mice that were treated in vitro with dexamethasone (Dex) during antigen restimulation exhibited reduced Th17 cytokine production, whereas Th17 cytokine production by lung cells from recipient mice of in vitro Th17-polarized OTII T-cells was resistant to Dex. These results demonstrate that the IL-1R/Th17 axis does not contribute to AHR development in NO2-promoted allergic airway disease, that Th17 adoptive transfer does not necessarily reflect an endogenously-generated Th17 response, and that functions of Th17 responses are contingent on the experimental conditions in which they are generated.

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Section: Discussionmentioning

confidence: 99%

The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

et al. 2013

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“…Therefore, we speculate that the higher levels of IFN‐γ in our airway inflammation model might be the major cause for inducing higher AHR responses by cell transfer of Th1 cells with OVA but without further administration of LPS though commercially available OVA contained negligible levels of endotoxin. Previous studies demonstrated that IFN‐γ was an important factor to induce AHR 13, 31–37, however, the precise mechanism of AHR induction by IFN‐γ remained unclear. As shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

IFN‐γ elevates airway hyper‐responsiveness via up‐regulation of neurokinin A/neurokinin‐2 receptor signaling in a severe asthma model

et al. 2011

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The adoptive transfer of OVA-specific Th1 cells into WT mice followed by OVA inhalation induces a significant elevation of airway hyper-responsiveness (AHR) with neutrophilia but not mucus hypersecretion. Here, we demonstrate that the airway inflammation model, pathogenically characterized as severe asthma, was partly mimicked by i.n. administration of IFN-c. The administration of IFN-c instead of Th1 cells caused AHR elevation but not neutrophilia, and remarkably induced neurokinin-2 receptor (NK2R) expression along with neurokinin A (NKA) production in the lung. To evaluate whether NKA/NK2R was involved in airway inflammation, we first investigated the role of NKA/NK2R-signaling in airway smooth muscle cells (ASMCs) in vitro. NK2R mRNA expression was significantly augmented in tracheal tube-derived ASMCs of WT mice but not STAT-1 À/À mice after stimulation with IFN-c. In addition, methacholine-mediated Ca 21 influx into the ASMCs was significantly reduced in the presence of NK2R antagonist. Moreover, the NK2R antagonist strongly inhibited IFN-c-dependent AHR elevation in vivo. Thus, these results demonstrated that IFN-c directly acts on ASMCs to elevate AHR via the NKA/NK2R-signaling cascade. Our present findings suggested that NK2R-mediated neuro-immuno crosstalk would be a promising target for developing novel drugs in Th1-cell-mediated airway inflammation, including severe asthma.

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“…The hormone vitellogenin, from Beluga caviar and salmon roe, has been shown to cause IgE reactivity [44,64]. Occupational allergy due to inhalation of heat-stable parasite allergens has also been shown to cause allergic reactions in fish-processing workers [68,73]. Fish contaminated with the parasitic nematode, Anisakis, may cause allergic reactions, where IgE is directed not at fish allergen, but at parasite proteins.…”

Section: Other Fish Allergensmentioning

confidence: 99%

“…A number of allergens have been characterized from Anisakis including tropomyosin and protease inhibitors. Occupational allergy due to inhalation of heat-stable parasite allergens has also been shown to cause allergic reactions in fish-processing workers [68,73].…”

Section: Other Fish Allergensmentioning

confidence: 99%

Allergenicity of bony and cartilaginous fish – molecular and immunological properties

Stephen

Sharp

Ruethers

et al. 2017

Clin Experimental Allergy

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Allergy to bony fish is common and probably increasing world-wide. The major heat-stable pan-fish allergen, parvalbumin (PV), has been identified and characterized for numerous fish species. In contrast, there are very few reports of allergic reactions to cartilaginous fish despite widespread consumption. The molecular basis for this seemingly low clinical cross-reactivity between these two fish groups has not been elucidated. PV consists of two distinct protein lineages, α and β. The α-lineage of this protein is predominant in muscle tissue of cartilaginous fish (Chondrichthyes), while β-PV is abundant in muscle tissue of bony fish (Osteichthyes). The low incidence of allergic reactions to ingested rays and sharks is likely due to the lack of molecular similarity, resulting in reduced immunological cross-reactivity between the two PV lineages. Structurally and physiologically, both protein lineages are very similar; however, the amino acid homology is very low with 47-54%. Furthermore, PV from ancient fish species such as the coelacanth demonstrates 62% sequence homology to leopard shark α-PV and 70% to carp β-PV. This indicates the extent of conservation of the PV isoforms lineages across millennia. This review highlights prevalence data on fish allergy and sensitization to fish, and details the molecular diversity of the two protein lineages of the major fish allergen PV among different fish groups, emphasizing the immunological and clinical differences in allergenicity.

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

Cited by 19 publications

References 44 publications

The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer

IFN‐γ elevates airway hyper‐responsiveness via up‐regulation of neurokinin A/neurokinin‐2 receptor signaling in a severe asthma model

Allergenicity of bony and cartilaginous fish – molecular and immunological properties

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