Please use this identifier to cite or link to this item: doi:10.22028/D291-36763
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Title: Blockade of PD-1 decreases neutrophilic inflammation and lung damage in experimental COPD
Author(s): Ritzmann, Felix
Borchardt, Kai
Vella, Giovanna
Chitirala, Praneeth
Angenendt, Adrian
Herr, Christian
Menger, Michael D.
Hoth, Markus
Lis, Annette
Bohle, Rainer M.
Bals, Robert
Beisswenger, Christoph
Language: English
Title: American Journal of Physiology. Lung Cellular and Molecular Physiology
Volume: 320
Issue: 5
Pages: L958–L968
Publisher/Platform: American Physiological Society
Year of Publication: 2021
Free key words: COPD
inflammation
lung damage
macrophages
PD-1
PD-L1
DDC notations: 610 Medicine and health
Publikation type: Journal Article
Abstract: Chronic obstructive lung disease (COPD) and lung cancer are both caused by smoking and often occur as comorbidity. The programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) axis is an important canonic immunoregulatory pathway, and antibodies that specifically block PD-1 or PD-L1 have demonstrated efficacy as therapeutic agents for non-small cell lung cancer. The role of the PD-1/PD-L1 axis in the pathogenesis of COPD is unknown. Here, we analyzed the function of the PD-1/PD-L1 axis in preclinical COPD models and evaluated the concentrations of PD-1 and PD-L1 in human serum and bronchoalveolar lavage (BAL) fluids as biomarkers for COPD. Anti-PD-1 treatment decreased lung damage and neutrophilic inflammation in mice chronically exposed to cigarette smoke (CS) or nontypeable Haemophilus influenzae (NTHi). Ex vivo stimulated macrophages obtained from anti-PD-1-treated mice released reduced amounts of inflammatory cytokines. PD-L1 concentrations correlated positively with PD-1 concentrations in human serum and BAL fluids. Lung sections obtained from patients with COPD stained positive for PD-L1. Our data indicate that the PD-1/PD-L1 axis is involved in developing inflammation and tissue destruction in COPD. Inflammation-induced activation of the PD-1 pathway may contribute to disease progression.
DOI of the first publication: 10.1152/ajplung.00121.2020
URL of the first publication: https://journals.physiology.org/doi/full/10.1152/ajplung.00121.2020
Link to this record: urn:nbn:de:bsz:291--ds-367634
hdl:20.500.11880/33404
http://dx.doi.org/10.22028/D291-36763
ISSN: 1522-1504
1040-0605
Date of registration: 11-Jul-2022
Description of the related object: Supplemental material
Related object: https://figshare.com/ndownloader/files/26617658
Faculty: M - Medizinische Fakultät
Department: M - Biophysik
M - Chirurgie
M - Innere Medizin
M - Pathologie
Professorship: M - Prof. Dr. Robert Bals
M - Prof. Dr. Rainer M. Bohle
M - Prof. Dr. Markus Hoth
M - Prof. Dr. Michael D. Menger
Collections:Die Universitätsbibliographie

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