Pneumologie 2019; 73(S 01)
DOI: 10.1055/s-0039-1678316
Freie Vorträge (FV DGP 13) – Sektion Allergologie und Immunologie
Pneumologische Immunologie und Allergologie
Georg Thieme Verlag KG Stuttgart · New York

Influenza virus-induced expression of CCL5 in monocyte/T-cell co-cultures is reduced in COPD

L Betke
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
S Yanik
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
K Jamal Jameel
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
E Bülthoff
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
P Bürger
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
A Koch
2   Kliniken an der Paar, Krankenhaus Friedberg
,
N Giannakis
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
J Kronsbein
1   Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil, Medizinische Klinik III
,
M Tenbusch
3   Friedrich-Alexander-University of Erlangen-Nürnberg, Department of Clinical and Molecular Virology
,
J Knobloch
4   Medizinische Klinik III für Pneumologie, Allergologie, Schlaf- und Beatmungsmedizin; Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil
› Author Affiliations
Further Information

Publication History

Publication Date:
19 February 2019 (online)

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    Background COPD subjects have an increased susceptibility to viral infections that cause exacerbations. This implicates defects in immune responses. Systemic defects in circulating immune cells might prevent their full activation after recruitment to the airways in response to acute infections. Monocytes are antigen-presenting cells that can activate T-cells. Cytokine production is an activation marker. CCL5/RANTES recruits further T-cells to the sites of infection and protects macrophages from Influenza virus (IAV)-induced apoptosis thereby allowing for clearance of inflammation- and obstruction-causing cellular corpses.

    We hypothesized that IAV-induced cytokine production of monocytes and T-cells is reduced in COPD.

    Methods According to sample size calculation, pure monocytes and pure T-cells were isolated by negative selection from the peripheral blood of n = 10 never-smokers (NS), n = 10 current smokers without COPD (S), and n = 12 COPD subjects. Pure monocytes, pure T-cells (control), and an 1 : 10 monocyte/T-cell mixture were cultured and treated with different IAV H1N1 concentrations (MOI 0.01 – 1.0) for 24 h, 72 h and 7 days. IFNα, IFNγ, TNFα, IL1β, CCL2, CCL5, IL-6, IL-8 were analyzed by ELISA and compared between the groups.

    Results Baseline cytokine releases were not different between the groups. IAV did not induce any cytokine in pure T-cells. IAV induced IL-6 and TNFα but reduced IL-8 in pure monocytes (all p < 0.05) without differences between NS, S, and COPD. In monocyte/T-cell co-cultures, IAV induced CCL5, IFNγ (Th1/Tc1 marker) and IL-6 but suppressed IL-8 (all p < 0.05). The effects on IFNγ, IL-6 and IL-8 were without differences between the groups. However, IAV-induced CCL5 was reduced in COPD vs. NS and S (each p < 0.05).

    Discussion IAV activates monocytes. IAV-activated monocytes drive T-cells towards Th1/Tc1. IAV-induced CCL5 – most likely from T-cells – is reduced in COPD. This might cause reduced T-cell recruitment and macrophage activity in response to acute IAV infections in COPD and contribute to IAV-caused exacerbations.