Radiographic airway abnormalities in untreated early rheumatoid arthritis are associated with peripheral neutrophil activation.

Anti-citrullinated protein antibodies HRCT Neutrophil activation Pulmonary abnormalities Rheumatoid arthritis Rheumatoid factor

Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
20 03 2023
Historique:
received: 09 12 2022
accepted: 22 02 2023
entrez: 21 3 2023
pubmed: 22 3 2023
medline: 23 3 2023
Statut: epublish

Résumé

The role of the lung for the initiation and progression of rheumatoid arthritis (RA) is still unclear. Up to 10% of RA patients develop interstitial lung disease which remains a clinical challenge. Understanding early disease mechanisms is of great importance. The objective of this study was to determine whether there is an association between peripheral neutrophil phenotypes and presence of pulmonary abnormalities (PA) on chest high-resolution computed tomography (HRCT) in untreated early RA (ueRA). Clinical data and blood were collected, and HRCT performed at diagnosis on 30 consecutive anti-citrullinated protein antibody (ACPA) and/or rheumatoid factor (RF) positive ueRA patients. HRCTs were evaluated for the presence of RA-associated parenchymal, airway and/or pleural abnormalities. Expression of phenotype markers on neutrophils were determined by flow cytometry. Levels of calprotectin, ACPA and RF were measured using immunoassays. The frequency of having any PA was 60%. Airway abnormalities were present in 50%, parenchymal nodules in 43% and interstitial lung abnormalities (ILA) in 10%. Unsupervised multivariate data analysis showed clustering of any PA with neutrophil activation, parameters of inflammation and RF titres. In univariate analysis, the patients with PA displayed significantly increased CD11b and decreased CD62L expression on neutrophils (1.2-fold, p = 0.014; 0.8-fold, p = 0.012) indicating activation and significantly increased RF IgM titre and CRP (5.7-fold, p = 0.0025; 2.3-fold, p = 0.0035) as compared to no PA. Titres of RF, but not ACPA, correlated with expression of the neutrophil activation marker CD11b. A stratified analysis demonstrated that airway involvement was the PA subtype with the strongest association with neutrophil activation. We report a strong association between radiographic airway findings and activation of circulating neutrophils in early RA supporting a role of innate immunity and the lung at disease onset. Our results also indicate different contributions of RF and ACPA in the RA pathogenesis.

Sections du résumé

BACKGROUND
The role of the lung for the initiation and progression of rheumatoid arthritis (RA) is still unclear. Up to 10% of RA patients develop interstitial lung disease which remains a clinical challenge. Understanding early disease mechanisms is of great importance. The objective of this study was to determine whether there is an association between peripheral neutrophil phenotypes and presence of pulmonary abnormalities (PA) on chest high-resolution computed tomography (HRCT) in untreated early RA (ueRA).
METHODS
Clinical data and blood were collected, and HRCT performed at diagnosis on 30 consecutive anti-citrullinated protein antibody (ACPA) and/or rheumatoid factor (RF) positive ueRA patients. HRCTs were evaluated for the presence of RA-associated parenchymal, airway and/or pleural abnormalities. Expression of phenotype markers on neutrophils were determined by flow cytometry. Levels of calprotectin, ACPA and RF were measured using immunoassays.
RESULTS
The frequency of having any PA was 60%. Airway abnormalities were present in 50%, parenchymal nodules in 43% and interstitial lung abnormalities (ILA) in 10%. Unsupervised multivariate data analysis showed clustering of any PA with neutrophil activation, parameters of inflammation and RF titres. In univariate analysis, the patients with PA displayed significantly increased CD11b and decreased CD62L expression on neutrophils (1.2-fold, p = 0.014; 0.8-fold, p = 0.012) indicating activation and significantly increased RF IgM titre and CRP (5.7-fold, p = 0.0025; 2.3-fold, p = 0.0035) as compared to no PA. Titres of RF, but not ACPA, correlated with expression of the neutrophil activation marker CD11b. A stratified analysis demonstrated that airway involvement was the PA subtype with the strongest association with neutrophil activation.
CONCLUSION
We report a strong association between radiographic airway findings and activation of circulating neutrophils in early RA supporting a role of innate immunity and the lung at disease onset. Our results also indicate different contributions of RF and ACPA in the RA pathogenesis.

Identifiants

pubmed: 36941690
doi: 10.1186/s13075-023-03019-5
pii: 10.1186/s13075-023-03019-5
pmc: PMC10026468
doi:

Substances chimiques

Rheumatoid Factor 9009-79-4
Autoantibodies 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

44

Informations de copyright

© 2023. The Author(s).

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Auteurs

Tilia Selldén (T)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.

Carina Kärrman Mårdh (CK)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.
Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Martin Joelsson (M)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.
Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Jenny Vikgren (J)

Department of Radiology, Institute for Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Radiology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Åse Johnsson (Å)

Department of Radiology, Institute for Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Radiology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Gunilla Larsson (G)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.

Daniel Glinatsi (D)

Department of Rheumatology, Skaraborg Hospital, Skövde, Sweden.

Kajsa Stubendorff (K)

Department of Rheumatology, Skaraborg Hospital, Skövde, Sweden.

Karin Svensson (K)

Department of Rheumatology, Skaraborg Hospital, Skövde, Sweden.

Inger Gjertsson (I)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.
Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Anna Rudin (A)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.
Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Anna-Carin Lundell (AC)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden.

Anna-Karin Hultgård Ekwall (AH)

Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, Gothenburg, SE-405 30, Sweden. ak.ekwall@rheuma.gu.se.
Department of Rheumatology, Sahlgrenska University Hospital, Gothenburg, Sweden. ak.ekwall@rheuma.gu.se.

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Classifications MeSH