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Cytotoxic lymphocytes in COPD airways: increased NK cells associated with disease, iNKT and NKT-like cells with current smoking
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.ORCID iD: 0000-0003-4266-1782
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
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2018 (English)In: Respiratory Research, ISSN 1465-9921, E-ISSN 1465-993X, Vol. 19, article id 244Article in journal (Refereed) Published
Abstract [en]

Background: Cytotoxic lymphocytes are increased in the airways of COPD patients. Whether this increase is driven primarily by the disease or by smoking is not clear, nor whether it correlates with the rate of decline in lung function.

Methods: Bronchoscopy with BAL was performed in 52 subjects recruited from the longitudinal OLIN COPD study according to pre-determined criteria; 12 with COPD and a rapid decline in lung function (loss of FEV1 ≥ 60 ml/year), 10 with COPD and a non-rapid decline in lung function (loss of FEV1 ≤ 30 ml/year), 15 current and ex-smokers and 15 non-smokers with normal lung function. BAL lymphocyte subsets were determined using flow cytometry.

Results: In BAL fluid, the proportions of NK, iNKT and NKT-like cells all increased with pack-years. Within the COPD group, NK cells – but not iNKT or NKT-like cells – were significantly elevated also in subjects that had quit smoking. In contrast, current smoking was associated with a marked increase in iNKT and NKT-like cells but not in NK cells. Rate of lung function decline did not significantly affect any of the results.

Conclusions: In summary, increased proportions of NK cells in BAL fluid were associated with COPD; iNKT and NKT-like cells with current smoking but not with COPD. Interestingly, NK cell percentages did not normalize in COPD subjects that had quit smoking, indicating that these cells might play a role in the continued disease progression seen in COPD even after smoking cessation.

Trial registration: Clinicaltrials.gov identifier NCT02729220.

Place, publisher, year, edition, pages
BMC , 2018. Vol. 19, article id 244
Keywords [en]
Chronic obstructive pulmonary disease, Disease mechanisms, Lung function decline, Smoking habits, Bronchoalveolar lavage
National Category
Respiratory Medicine and Allergy
Identifiers
URN: urn:nbn:se:umu:diva-154873DOI: 10.1186/s12931-018-0940-7ISI: 000452747200001PubMedID: 30526599Scopus ID: 2-s2.0-85058092775OAI: oai:DiVA.org:umu-154873DiVA, id: diva2:1275163
Available from: 2019-01-04 Created: 2019-01-04 Last updated: 2019-01-04Bibliographically approved

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Eriksson Ström, JonasPourazar, JamshidLinder, RobertBlomberg, AndersLindberg, AnneBehndig, Annelie F.

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