Allergy and Airway: Asthma III |

The Role of IL-17A in the Pathogenesis of Early Infection With RSV Increasing Susceptibility to Asthma FREE TO VIEW

Zhijun Jie; Xiao Sun; Yanchao He, MD; Wei Sun; Jindong Shi
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The Fifth hospital of Shanghai, Shanghai, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A24. doi:10.1016/j.chest.2016.02.026
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE:The role of IL-17A in the pathogenesis of early infection with RSV increasing susceptibility to asthma.

METHODS: Establishing a mice model of immune tolerance by oral feeding with OVA, and infected with RSV before arousing airway high reactivity. Neutralizing IL-17A before infected with RSV. After the last challenge with OVA the mice were analyzed for AHR, eosinophil infiltration, levels of cytokines, IgE production, percentage of Th2 and Th17 cell, and lung histology.

RESULTS: After RSV infection, the Tol group developed the re-emergence of symptoms of asthma, such as increased airway pressure, elevated serum IgE and total number of inflammatory cells in BALF compared with non-infected tolerance group. Quantitative PCR showed that in Tol+RSV group, the mRNA expressions of IL-4, IL-5, IL-13 and IL-17A were significantly up-regulated, especially IL-17A. Pathological results showed that inflammatory responses of the lung reappeared again. Th2, Th17 subsets of hilar lymph nodes in infected mice and non-infected were 2.45±0.06% and 2.19%±0.05% respectively, significantly higher than control group (P <0.05). IL-17A neutralizing antibodies administrated to RSV infection mice significantly reduced airway hyperresponsiveness, serum IgE production and pathological inflammatory responses. Th2, Th17 subsets were also significantly lower than those of the infected control group.

CONCLUSIONS: Early RSV infection could break immune tolerance of oral OVA and re-induced asthma, which might be due to Th17/IL-17A up-regulation. IL-17 Ab could inhibit the damaging effects of early RSV infection to immune tolerance mice.

CLINICAL IMPLICATIONS: RhIL-17A may be therapeutically in non-eosinophilic asthma and refractory asthma.

DISCLOSURE: The following authors have nothing to disclose: Zhijun Jie, Xiao Sun, Yanchao He, Wei Sun, Jindong Shi

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