| First Author | McCubbrey AL | Year | 2016 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 311 |
| Issue | 1 | Pages | L87-L100 |
| PubMed ID | 27190063 | Mgi Jnum | J:236056 |
| Mgi Id | MGI:5804510 | Doi | 10.1152/ajplung.00141.2016 |
| Citation | McCubbrey AL, et al. (2016) Selective and inducible targeting of CD11b+ mononuclear phagocytes in the murine lung with hCD68-rtTA transgenic systems. Am J Physiol Lung Cell Mol Physiol 311(1):L87-L100 |
| abstractText | During homeostasis two distinct macrophage (Mo) populations inhabit the lungs: tissue Mo (often called interstitial Mo) and resident alveolar Mo (resAMo). During acute lung inflammation, monocytes from the circulation migrate to areas of injury where they mature into a third Mo population: recruited Mo. Resident AMo uniquely express low levels of CD11b and high levels of CD11c. In comparison, recruited Mo and tissue Mo express high levels of CD11b and low levels of CD11c. It is likely that these three Mo 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 Mo and tissue Mo in the murine lung with negligible activation in resAMo. Using hCD68rtTA-GFP reporter mice, we show both during homeostasis and inflammation that administration of doxycycline induces tet-On reporter expression in recruited Mo and tissue Mo but not in resident AMo. We further demonstrate how hCD68-rtTA can be effectively combined with tet-On Cre to target these same recMo and tissue Mo. 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(+) Mo during lung heath and disease. |
