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Biomarkers for Comorbidities Modulate the Activity of T-Cells in COPD

Medical Clinic III for Pneumology, Allergology and Sleep Medicine, Bergmannsheil University Hospital, Ruhr-University Bochum, Bürkle-de-la-Camp-Platz 1, 44789 Bochum, Germany
Department of Internal Medicine II, Pneumology, Allergology and Respiratory Medicine, Bethel Teaching Hospital, 12207 Berlin, Germany
Pyhrn-Eisenwurzen-Klinikum Steyr, Klinik für Pneumologie, Lehrkrankenhaus der Uniklinik Linz, Sierninger Str. 170, 4400 Steyr, Austria
Ludwig-Maximilians-University of Munich (LMU) and DZL (German Center of Lung Science), 81377 Munich, Germany
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editors: Yuji Takeda and Massimo Conese
Int. J. Mol. Sci. 2021, 22(13), 7187;
Received: 26 April 2021 / Revised: 17 June 2021 / Accepted: 27 June 2021 / Published: 2 July 2021
(This article belongs to the Special Issue The Role of Interleukin in Health and Diseases)
In smoking-induced chronic obstructive pulmonary disease (COPD), various comorbidities are linked to systemic inflammation and infection-induced exacerbations. The underlying mechanisms are unclear but might provide therapeutic targets. T-cell activity is central in systemic inflammation and for infection-defense mechanisms and might be influenced by comorbidities. Hypothesis: Circulating biomarkers of comorbidities modulate the activity of T-cells of the T-helper type 1 (Th1) and/or T-cytotoxic type 1 (Tc1). T-cells in peripheral blood mononuclear cells (PBMCs) from non-smokers (NS), current smokers without COPD (S), and COPD subjects (total n = 34) were ex vivo activated towards Th1/Tc1 and were then stimulated with biomarkers for metabolic and/or cardiovascular comorbidities (Brain Natriuretic Peptide, BNP; chemokine (C-C motif) ligand 18, CCL18; C-X3-C motif chemokine ligand 1, CX3CL1; interleukin-18, IL-18) or for asthma- and/or cancer-related comorbidities (CCL22; epidermal growth factor, EGF; IL-17; periostin) each at 10 or 50 ng/mL. The Th1/Tc1 activation markers interferon-γ (IFNγ), tumor necrosis factor-α (TNFα), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were analyzed in culture supernatants by Enzyme-Linked Immunosorbent Assay (ELISA). Ex-vivo activation induced IFNγ and TNFα without differences between the groups but GM-CSF more in S vs. NS. At 10 ng/mL, the different biomarkers increased or reduced the T-cell activation markers without a clear trend for one direction in the different categories of comorbidities or for the different T-cell activation markers. At 50 ng/mL, there was a clear shift towards suppressive effects, particularly for the asthma— and cancer-related biomarkers and in cells of S and COPD. Comorbidities might suppress T-cell immunity in COPD. This could explain the association of comorbidities with frequent exacerbations. View Full-Text
Keywords: COPD; comorbidities; T-cells COPD; comorbidities; T-cells
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MDPI and ACS Style

Jamal Jameel, K.; Gallert, W.-J.; Yanik, S.D.; Panek, S.; Kronsbein, J.; Jungck, D.; Koch, A.; Knobloch, J. Biomarkers for Comorbidities Modulate the Activity of T-Cells in COPD. Int. J. Mol. Sci. 2021, 22, 7187.

AMA Style

Jamal Jameel K, Gallert W-J, Yanik SD, Panek S, Kronsbein J, Jungck D, Koch A, Knobloch J. Biomarkers for Comorbidities Modulate the Activity of T-Cells in COPD. International Journal of Molecular Sciences. 2021; 22(13):7187.

Chicago/Turabian Style

Jamal Jameel, Kaschin, Willem-Jakob Gallert, Sarah D. Yanik, Susanne Panek, Juliane Kronsbein, David Jungck, Andrea Koch, and Jürgen Knobloch. 2021. "Biomarkers for Comorbidities Modulate the Activity of T-Cells in COPD" International Journal of Molecular Sciences 22, no. 13: 7187.

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