Functional characterization of small and large alveolar macrophages in sarcoidosis and idiopathic pulmonary fibrosis compared with non-fibrosis interstitial lung diseases.

Sarcoidosis idiopathic pulmonary fibrosis large alveolar macrophages non-fibrosis ILDs small alveolar macrophages

Journal

Human antibodies
ISSN: 1875-869X
Titre abrégé: Hum Antibodies
Pays: Netherlands
ID NLM: 9711270

Informations de publication

Date de publication:
2023
Historique:
pubmed: 14 8 2023
medline: 14 8 2023
entrez: 14 8 2023
Statut: ppublish

Résumé

Sarcoidosis is a granulomatous disease that mostly affects the lungs. Advanced tissue injury caused by this disease can progress to pulmonary fibrosis with similar characteristics shared with idiopathic pulmonary fibrosis (IPF). The initial presentations of both sarcoidosis and IPF may be shared with other interstitial lung diseases (ILDs). Two populations of macrophages have been described in the alveolar space: small alveolar macrophages (AMs) and large alveolar macrophages. Despite their protective function, these cells may also play a role in the initiation and maintenance of inflammation leading to fibrosis. The aim of this study was the functional characterization of small and large AM subpopulations in sarcoidosis and IPF as a pathology with respectively mild and advanced tissue injury causing fibrosis, in comparison with non-fibrosis ILDs. Activation and adhesion surface markers as well as functions of small and large AMs isolated from bronchoalveolar lavage (BAL) were assessed by Flow Cytometry within patients with confirmed sarcoidosis (n= 14), IPF (n= 6), and non-fibrosis ILDs (n= 9). Our results showed that small AMs are immunologically more active, which may be important for airway inflammation. They are also proportionally more abundant in IPF, and therefore they may be more involved in a fibrosis process associated with the down-regulation of HLA-DR, LeuCAM, and CD62L expression. In Sarcoidosis, the inflammatory process appears to be associated with up-regulation of CD38 expression and oxidative burst activity. A relevant potential of the activation and adhesion markers as well as oxidative burst activity expressed on small and large AMs, in the perspective of differential diagnosis of sarcoidosis and IPF.

Sections du résumé

BACKGROUND BACKGROUND
Sarcoidosis is a granulomatous disease that mostly affects the lungs. Advanced tissue injury caused by this disease can progress to pulmonary fibrosis with similar characteristics shared with idiopathic pulmonary fibrosis (IPF). The initial presentations of both sarcoidosis and IPF may be shared with other interstitial lung diseases (ILDs). Two populations of macrophages have been described in the alveolar space: small alveolar macrophages (AMs) and large alveolar macrophages. Despite their protective function, these cells may also play a role in the initiation and maintenance of inflammation leading to fibrosis.
OBJECTIVE OBJECTIVE
The aim of this study was the functional characterization of small and large AM subpopulations in sarcoidosis and IPF as a pathology with respectively mild and advanced tissue injury causing fibrosis, in comparison with non-fibrosis ILDs.
METHODS METHODS
Activation and adhesion surface markers as well as functions of small and large AMs isolated from bronchoalveolar lavage (BAL) were assessed by Flow Cytometry within patients with confirmed sarcoidosis (n= 14), IPF (n= 6), and non-fibrosis ILDs (n= 9).
RESULTS RESULTS
Our results showed that small AMs are immunologically more active, which may be important for airway inflammation. They are also proportionally more abundant in IPF, and therefore they may be more involved in a fibrosis process associated with the down-regulation of HLA-DR, LeuCAM, and CD62L expression. In Sarcoidosis, the inflammatory process appears to be associated with up-regulation of CD38 expression and oxidative burst activity.
CONCLUSION CONCLUSIONS
A relevant potential of the activation and adhesion markers as well as oxidative burst activity expressed on small and large AMs, in the perspective of differential diagnosis of sarcoidosis and IPF.

Identifiants

pubmed: 37574726
pii: HAB230005
doi: 10.3233/HAB-230005
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

59-69

Auteurs

Sara El Fakihi (S)

, Rabat, Morocco.
Medical Biotechnology Laboratory, Faculty of Medicine and Pharmacy, University Mohammed V, Rabat, Morocco.

Aicha El Allam (A)

, Rabat, Morocco.
Department of Immunology, School of Medicine, Yale University, New Haven, CT, USA.

Hicham Tahoune (H)

, Rabat, Morocco.
Department of Microbiology, CHU Mohammed VI, Tangier, Morocco.

Nouhaila Najimi (N)

, Rabat, Morocco.
Laboratory of Human Pathologies, Department of Biology, Faculty of Sciences, University Mohammed V, Rabat, Morocco.

Chaimae Kadi (C)

, Rabat, Morocco.
Department of Biology, Faculty of Sciences, University Abdelmalek Essaadi, Tetouan, Morocco.

Azeddine Ibrahimi (A)

, Rabat, Morocco.
Medical Biotechnology Laboratory, Faculty of Medicine and Pharmacy, University Mohammed V, Rabat, Morocco.

Jamal-Eddine Bourkadi (JE)

Pneumo-Phtisiology Department, Moulay Youssef Hospital, Rabat, Morocco.
Faculty of Medicine and Pharmacy, University Mohammed V, Rabat, Morocco.

Fouad Seghrouchni (F)

, Rabat, Morocco.

Classifications MeSH