2019Unpublished venueRequires access

IL-4, IL-8, IL-13, IL-17, IL-33 serum levels changes in acute allergic asthma model

Virginija Kalinauskaitė-Žukauskė, Andrius Januškevičius, Ieva Janulaitytė, Kęstutis Malakauskas

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Abstract

Background: Type 2 inflammation plays a pivotal role in the pathogenesis of eosinophilic asthma. Cytokines are crucial in orchestrating, perpetuating and amplifying the airway inflammatory response. Currently, there is a lack of data about their changes in an acute asthma attack. Aim: to investigate serum levels of cytokines IL-4, IL-8, IL-13, IL-17, IL-33 in acute allergic asthma (AA). Methods: We examined 16 patients: 8 steroid-free, stable, sensitized to Dermatophagoides pteronyssinus patients with AA and 8 healthy, non-atopic subjects (HS). Bronchial allergen challenge was performed using inhaled D. pteronyssinus (Diater, Spain) via a pressure dosimeter (ProvoX, Ganshorn, Germany). Cytokines levels in serum were measured by ELISA before allergen challenge (V1) and after 24 hours (V2). Results: at the baseline (V1) patients from the AA group had higher serum levels of IL-4, IL-8, IL-13 and IL-33 compared to HS (table). After allergen challenge levels of IL-4, IL-8, IL-13 and IL-17 significantly increased only in the AA group. *p<0.05, compared to HS at the same visit; NS – not significant. Conclusion: Type 2 inflammation–derived cytokines IL-4, IL-8, IL-13 and IL-17 are involved in early-onset eosinophilic airway inflammation in acute AA.

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What this paper is about

Background: Type 2 inflammation plays a pivotal role in the pathogenesis of eosinophilic asthma. Cytokines are crucial in orchestrating, perpetuating and amplifying the airway inflammatory response. Currently, there is a lack of data about their changes in an acute asthma attack. Aim: to investigate serum levels of cytokines IL-4, IL-8, IL-13, IL-17, IL-33 in acute allergic asthma (AA). Methods: We examined 16 patients: 8 steroid-free, stable, sensitized to Dermatophagoides pteronyssinus patients with AA and 8 healthy, non-atopic subjects (HS). Bronchial allergen challenge was performed using inhaled D. pteronyssinus (Diater, Spain) via a pressure dosimeter (ProvoX, Ganshorn, Germany). Cytokines levels in serum were measured by ELISA before allergen challenge (V1) and after 24 hours (V2). Results: at the baseline (V1) patients from the AA group had higher serum levels of IL-4, IL-8, IL-13 and IL-33 compared to HS (table). After allergen challenge levels of IL-4, IL-8, IL-13 and IL-17 significantly increased only in the AA group. *p<0.05, compared to HS at the same visit; NS – not significant. Conclusion: Type 2 inflammation–derived cytokines IL-4, IL-8, IL-13 and IL-17 are involved in early-onset eosinophilic airway inflammation in acute AA.

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Available abstract

Background: Type 2 inflammation plays a pivotal role in the pathogenesis of eosinophilic asthma. Cytokines are crucial in orchestrating, perpetuating and amplifying the airway inflammatory response. Currently, there is a lack of data about their changes in an acute asthma attack. Aim: to investigate serum levels of cytokines IL-4, IL-8, IL-13, IL-17, IL-33 in acute allergic asthma (AA). Methods: We examined 16 patients: 8 steroid-free, stable, sensitized to Dermatophagoides pteronyssinus patients with AA and 8 healthy, non-atopic subjects (HS). Bronchial allergen challenge was performed using inhaled D. pteronyssinus (Diater, Spain) via a pressure dosimeter (ProvoX, Ganshorn, Germany). Cytokines levels in serum were measured by ELISA before allergen challenge (V1) and after 24 hours (V2). Results: at the baseline (V1) patients from the AA group had higher serum levels of IL-4, IL-8, IL-13 and IL-33 compared to HS (table). After allergen challenge levels of IL-4, IL-8, IL-13 and IL-17 significantly increased only in the AA group. *p<0.05, compared to HS at the same visit; NS – not significant. Conclusion: Type 2 inflammation–derived cytokines IL-4, IL-8, IL-13 and IL-17 are involved in early-onset eosinophilic airway inflammation in acute AA.

Key concepts: Medicine, Asthma, Immunology, Interleukin 13, Pathogenesis, Inflammation, Allergen, Allergy

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