Extract
Both sarcoidosis and chronic beryllium disease (CBD) are granulomatous diseases with overlapping clinical features; however, their clinical courses differ. CBD may have slow clinical progression and rarely resolves, while sarcoidosis has variable progression and may resolve depending on the stage of the disease [1]. These commonalities and differences imply differences in antigen(s), and potentially clearance and persistence. Alveolar macrophages play an important role in this process, driving innate [2] and adaptive immune responses [3]. Furthermore, subpopulations of macrophages may promote granulomatous inflammation and resolution of lung injury [4], key aspects of sarcoidosis and CBD. Using single-cell RNA sequencing (scRNA-seq), we explored the common and unique pathways between progressive (SarcP) and remitting (SarcR) sarcoidosis as well as CBD and sarcoidosis, focusing on macrophages and macrophage subpopulations (recruited versus resident).
Abstract
scRNA-seq characterised macrophage transcriptional and chromatin accessibility profiles in BAL cells in granulomatous lung diseases, chronic beryllium disease and sarcoidosis, and identified signatures of disease progression in sarcoidosis. https://bit.ly/3piFIBy
Footnotes
Conflict of interest: S-Y. Liao has nothing to disclose. S.M. Atif has nothing to disclose.
Conflict of Interest: S.M. Atif has nothing to disclose.
Conflict of interest: K. Mould has nothing to disclose.
Conflict of interest: I.R. Konigsberg has nothing to disclose.
Conflict of interest: R. Fu has nothing to disclose.
Conflict of interest: E. Davidson has nothing to disclose.
Conflict of interest: L. Li has nothing to disclose.
Conflict of interest: A.P. Fontenot reports grants from National Institutes of Health (NIH; HL62410, HL152756, HL102245, and ES025534), during the conduct of the study.
Conflict of interest: L.A. Maier reports grants from National Institutes of Health (1R01 HL140357-01A1, “Epigenetic Regulation of Immune Pathways in Sarcoidosis”; 1R01 ES023826-01A1, “Exposure in Epigenetic Regulation of Immune Response in CBD”), during the conduct of the study; grants from National Institutes of Health (1R01 HL127461-01A1, 1R01 ES025534-01A1, 1R01ES025722-01A1, R01HL136681-01A1, UL1TRR002535, R01HL136681-01A1, 1R01 HL152756-01), grants from University of Cincinnati under a Mallinckrodt Foundation (“Registry for Sarcoidosis Associated Hypertension”, “Registry for Advanced Sarcoidosis”), grants from MNK14344100 (A Phase 4 Multicenter, Randomized, Double Blind, Placebo Controlled Pilot Study to Assess the Efficacy and Safety of H.P. Acthar Gel in Subjects with Pulmonary Sarcoidosis), grants from ATYR1923-C-002 (A Randomized, Double-Blind, Placebo-Controlled Multiple Ascending Dose Study of Intravenous ATYR1923 in Patients with Pulmonary Sarcoidosis), outside the submitted work; and is a member of the FSR Scientific Advisory Board, but does not receive any compensation for this activity.
Conflict of interest: I.V. Yang reports grants from NIH, during the conduct of the study and personal fees from Eleven P15 for consultancy, outside the submitted work; and has a patent Circulating Biomarkers of Preclinical Pulmonary Fibrosis pending.
Support statement: NIH-NIEHS R01-ES023826, NIH-NHLBI R01-HL140357, University of Colorado RNA Biosciences Initiative (all to L.A. Maier and I.V. Yang), and Foundation for Sarcoidosis Research Fellowship (to S-Y. Liao). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received October 9, 2020.
- Accepted February 8, 2021.
- Copyright ©The authors 2021. For reproduction rights and permissions contact permissions{at}ersnet.org