Selective and inducible targeting of CD11b+mononuclear phagocytes in the murine lung with hCD68-rtTA transgenic systems
Open accessAbstract
During homeostasis two distinct macrophage (Mø) populations inhabit the lungs: tissue Mø (often called interstitial Mø) and resident alveolar Mø (resAMø). During acute lung inflammation, monocytes from the circulation migrate to areas of injury where they mature into a third Mø population: recruited Mø. Resident AMø uniquely express low levels of CD11b and high levels of CD11c. In comparison, recruited Mø and tissue Mø express high levels of CD11b and low levels of CD11c. It is likely that these three Mø subpopulations play distinct roles in injury and disease states; however, tools with which to individually target or track these populations are lacking. Here we demonstrate the utility of an hCD68-rtTA transgenic system for specific, robust, and inducible targeting of CD11b+recruited Mø and tissue Mø in the murine lung with negligible activation in resAMø. Using hCD68rtTA-GFP reporter mice, we show both during homeostasis and inflammation that administration of doxycycline induces tet-On reporter expression in recruited Mø and tissue Mø but not in resident AMø. We further demonstrate how hCD68-rtTA can be effectively combined with tet-On Cre to target these same recMø and tissue Mø. Accordingly, the hCD68-rtTA system is a powerful new tool that can be used for lineage tracing, fate mapping, and gene deletion in a variety of murine models, thereby enabling sophisticated investigation of the unique role of these CD11b+Mø during lung heath and disease.
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Only Mo-AMs, not the entire type of cells, are responsible for the detrimental role of lung macrophages in pulmonary fibrosis.
“Recent studies have made inroads into this challenge by demonstrating that it is only a subgroup, the Mo-AMs, and not the entire type of cells, that are responsible for the detrimental role of lung macrophages in pulmonary fibrosis1,3,10,13.”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [10]
The introductory passage (page unavailable) distinguishes resident from recruited alveolar macrophages and says they can have different, even antagonistic, roles in lung injury. The paper does not establish that only monocyte-derived alveolar macrophages cause the detrimental macrophage effects in pulmonary fibrosis; its bleomycin results concern targeting these cells, not their causal role. (LLM, conf=0.82)
Experimental — accuracy not yet measuredMo-AMs, but not TR-AMs, are responsible for the pro-fibrotic activity of lung macrophages.
“Mo-AMs, but not TR-AMs, are responsible for the pro-fibrotic activity of this group of cells1,3,10,13”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [10]
The Abstract says recruited and resident alveolar macrophages may have distinct roles in lung injury, but does not assign pro-fibrotic activity to either group. In the bleomycin-injury results (page not available), the measured difference is hCD68-rtTA activation, not fibrosis-promoting function. Searches for pro-fibrotic activity and fibrosis did not find the claimed comparison. (LLM, conf=0.72)
Experimental — accuracy not yet measuredDepletion of Mo-AMs confers protection from lung fibrosis in multiple mouse models.
“depletion of Mo-AMs via several strategies conferred protection from lung fibrosis in multiple mouse models1,3,10,11,13,20”
From TREM2 promotes lung fibrosis via controlling alveolar macrophage survival and pro-fibrotic activity (2025) · cites this paper as [10]
Figure 10 and the accompanying results report activation of a reporter in recruited macrophages after bleomycin injury, not depletion or protection from fibrosis. The Discussion proposes manipulating recruited-macrophage survival as a future experiment. Searches for depletion and fibrosis did not find the claimed protective effect in multiple mouse models. (LLM, conf=0.75)
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- Authors
- McCubbrey, A. L., Barthel, L., Mould, K. J., Mohning, M. P., Redente, E. F., & Janssen, W. J.
- Affiliations
- National Jewish Health (US)
- Corresponding author
- McCubbrey, Alexandra L.
- ORCID
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2016-07-01
- Volume
- 311
- Issue
- 1
- Pages
- L87-L100
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- PMC
- PMC4967193
- OpenAlex
- W2396383474
- Cited by
- 17
- References
- 54
- Citations by year
- 2026: 1 · 2025: 2 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 1 · 2018: 2 · 2017: 5
- FWCI
- 1.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- HHS | National Institutes of Health (NIH) (HL109517, HL114381, HL007085-41, HL126333)
- Pulmonary Fibrosis Foundation (PFF)
- Francis Family Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- lung macrophages, alveolar macrophages, tissue macrophages, lineage tracing, fate mapping, doxycycline, acute lung inflammation, transgenic reporter mice
- MeSH terms
- CD68 Molecule, Animals, Lipopolysaccharides, Lung, Mice, Inbred C57BL, Mice, Transgenic, Organ Specificity, Phagocytes, Pneumonia, Antigens, Differentiation, Myelomonocytic, Transcriptional Activation, Antigens, CD, Gene Expression, CD11b Antigen
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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