Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types?
The onset of chronic obstructive pulmonary disease (COPD) is heterogeneous, and current approaches to define distinct disease phenotypes are lacking. In addition to clinical methodologies, subtyping COPD has also been challenged by the reliance on human lung samples from late-stage diseases. Different COPD phenotypes may be initiated from the susceptibility of different cell types to cigarette smoke, environmental pollution, and infections at early stages that ultimately converge at later stages in airway remodeling and destruction of the alveoli when the disease is diagnosed. This perspective provides discussion points on how studies to date define different cell types of the lung that can initiate COPD pathogenesis, focusing on the susceptibility of macrophages, T and B cells, mast cells, dendritic cells, endothelial cells, and airway epithelial cells. Additional cell types, including fibroblasts, smooth muscle cells, neuronal cells, and other rare cell types not covered here, may also play a role in orchestrating COPD. Here, we discuss current knowledge gaps, such as which cell types drive distinct disease phenotypes and/or stages of the disease and which cells are primarily affected by the genetic variants identified by whole genome-wide association studies. Applying new technologies that interrogate the functional role of a specific cell type or a combination of cell types as well as single-cell transcriptomics and proteomic approaches are creating new opportunities to understand and clarify the pathophysiology and thereby the clinical heterogeneity of COPD.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:69 |
|---|---|
| Enthalten in: |
American journal of respiratory cell and molecular biology - 69(2023), 5 vom: 01. Nov., Seite 500-507 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Tesfaigzi, Yohannes [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 02.11.2023 Date Revised 15.03.2024 published: Print Citation Status MEDLINE |
|---|
| doi: |
10.1165/rcmb.2023-0175PS |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM360839371 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM360839371 | ||
| 003 | DE-627 | ||
| 005 | 20240315232717.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1165/rcmb.2023-0175PS |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1330.xml |
| 035 | |a (DE-627)NLM360839371 | ||
| 035 | |a (NLM)37584669 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Tesfaigzi, Yohannes |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types? |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 02.11.2023 | ||
| 500 | |a Date Revised 15.03.2024 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a The onset of chronic obstructive pulmonary disease (COPD) is heterogeneous, and current approaches to define distinct disease phenotypes are lacking. In addition to clinical methodologies, subtyping COPD has also been challenged by the reliance on human lung samples from late-stage diseases. Different COPD phenotypes may be initiated from the susceptibility of different cell types to cigarette smoke, environmental pollution, and infections at early stages that ultimately converge at later stages in airway remodeling and destruction of the alveoli when the disease is diagnosed. This perspective provides discussion points on how studies to date define different cell types of the lung that can initiate COPD pathogenesis, focusing on the susceptibility of macrophages, T and B cells, mast cells, dendritic cells, endothelial cells, and airway epithelial cells. Additional cell types, including fibroblasts, smooth muscle cells, neuronal cells, and other rare cell types not covered here, may also play a role in orchestrating COPD. Here, we discuss current knowledge gaps, such as which cell types drive distinct disease phenotypes and/or stages of the disease and which cells are primarily affected by the genetic variants identified by whole genome-wide association studies. Applying new technologies that interrogate the functional role of a specific cell type or a combination of cell types as well as single-cell transcriptomics and proteomic approaches are creating new opportunities to understand and clarify the pathophysiology and thereby the clinical heterogeneity of COPD | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a gene-and-environment interaction | |
| 650 | 4 | |a lineage tracing | |
| 650 | 4 | |a lung cell types | |
| 650 | 4 | |a single nucleotide polymorphisms | |
| 650 | 4 | |a single-cell transcriptomics | |
| 700 | 1 | |a Curtis, Jeffrey L |e verfasserin |4 aut | |
| 700 | 1 | |a Petrache, Irina |e verfasserin |4 aut | |
| 700 | 1 | |a Polverino, Francesca |e verfasserin |4 aut | |
| 700 | 1 | |a Kheradmand, Farrah |e verfasserin |4 aut | |
| 700 | 1 | |a Adcock, Ian M |e verfasserin |4 aut | |
| 700 | 1 | |a Rennard, Stephen I |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t American journal of respiratory cell and molecular biology |d 1989 |g 69(2023), 5 vom: 01. Nov., Seite 500-507 |w (DE-627)NLM012606170 |x 1535-4989 |7 nnns |
| 773 | 1 | 8 | |g volume:69 |g year:2023 |g number:5 |g day:01 |g month:11 |g pages:500-507 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1165/rcmb.2023-0175PS |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 69 |j 2023 |e 5 |b 01 |c 11 |h 500-507 | ||