Pneumologie 2020; 74(S 01): 10-11
DOI: 10.1055/s-0039-3403076
Freie Vorträge (FV03) – Sektion Allergologie und Immunologie
Freie Vorträge der Sektion Allergologie und Immunologie
Georg Thieme Verlag KG Stuttgart · New York

The cytokine response of circulating immune cells to rhinovirus is reduced in severe asthma

K Jamal Jameel
1   Medical Clinic III, Bergmannsheil University Hospital
,
S Yanik
2   Klinik III für Pneumologie, Allergologie, Schlaf- und Beatmungsmedizin, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil Bochum
,
E Bülthoff
1   Medical Clinic III, Bergmannsheil University Hospital
,
F Yusuf
1   Medical Clinic III, Bergmannsheil University Hospital
,
B Struck
1   Medical Clinic III, Bergmannsheil University Hospital
,
S Rohde
1   Medical Clinic III, Bergmannsheil University Hospital
,
K Pfeifer
1   Medical Clinic III, Bergmannsheil University Hospital
,
J Kronsbein
2   Klinik III für Pneumologie, Allergologie, Schlaf- und Beatmungsmedizin, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil Bochum
,
A Koch
3   Clinic Davos, Zürcher Reha-Zentren
,
M Tenbusch
4   Department of Molecular and Medical Virology, Ruhr-University Bochum; Department of Clinical and Molecular Virology, University Hospital Erlangen
,
J Knobloch
2   Klinik III für Pneumologie, Allergologie, Schlaf- und Beatmungsmedizin, Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil Bochum
› Author Affiliations
Further Information

Publication History

Publication Date:
28 February 2020 (online)

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Background: Exacerbations trigger the progression of severe asthma and are often caused by airway infections with human rhinovirus (HRV). Asthma subjects are more susceptible to viral infections than healthy subjects. This suggests defects in the immune response to HRV. In response to HRV infections, circulating immune cells become recruited to and activated in the infected lung tissue and in the draining lymph nodes.

Hypothesis: The activation of circulating immune cells in response to HRV is impaired in severe asthma and is influenced by Typ2 inflammation.

Methods: Peripheral blood mononuclear cells (PBMCs) were isolated from 34 non-smokers with severe asthma (SA) and 19 healthy never-smokers (NS), cultivated and infected with HRV (strain 16) at MOI 0.1 and 1.0. After 24 h and 7 d, cytokines (activity markers) were measured by ELISA. Baseline-normalized data were compared between NS and SA and were analyzed for spearman correlation with total IgE (n = 31 SA) and with markers for Typ2 inflammation: blood eosinophils (n = 32 SA), serum-periostin (n = 29 SA), and FeNO (n = 25 SA).

Results: Baseline IL1β was increased and baseline IFNγ, IL6, IL8 and TNFα were reduced in SA vs. NS. HRV induced CCL2, CCL5, IFNα, IL1β, IL6 and TNFα after 24 h and 7 d and IFNγ and IL8 after 7 d in NS. The HRV-induced responses of all these cytokines except IFNγ were reduced in SA vs. NS. The IL6 response was lower in SA with < 300 than in SA with ≥ 300 eosinophils/µl blood. In SA, HRV-induced IFNα or IL1β or CCL2 correlated negatively to FeNO or periostin or both, respectively.

Conclusion: The cytokine response to HRV is reduced in PBMCs of severe asthma. This suggests systemic immune defects resulting in an impaired activation of circulating immune cells after recruitment to the infected tissue. This molecular pathology might be influenced by the intensity of Typ2 inflammation. The data can explain the impaired infection defense and the increased susceptibility to viral infections in asthma.