Hogg, Chloe and Panir, Kavita and Dhami, Priya and Rosser, Matthew and Mack, Matthias and Soong, Daniel and Pollard, Jeffrey W. and Jenkins, Stephen J. and Horne, Andrew W. and Greaves, Erin (2021) Macrophages inhibit and enhance endometriosis depending on their origin. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 118 (6): e201377611. ISSN 0027-8424,
Full text not available from this repository. (Request a copy)Abstract
Macrophages are intimately involved in the pathophysiology of endometriosis, a chronic inflammatory disorder characterized by the growth of endometrial-like tissue (lesions) outside the uterus. By combining genetic and pharmacological monocyte and macrophage depletion strategies we determined the ontogeny and function of macrophages in a mouse model of induced endometriosis. We demonstrate that lesion-resident macrophages are derived from eutopic endometrial tissue, infiltrating large peritoneal macrophages (LpM) and monocytes. Furthermore, we found endometriosis to trigger continuous recruitment of monocytes and expansion of CCR2+ LpM. Depletion of eutopic endometrial macrophages results in smaller endometriosis lesions, whereas constitutive inhibition of monocyte recruitment significantly reduces peritoneal macrophage populations and increases the number of lesions. Reprogramming the ontogeny of peritoneal macrophages such that embryo-derived LpM are replaced by monocyte-derived LpM decreases the number of lesions that develop. We propose a putative model whereby endometrial macrophages are "proendometriosis" while newly recruited monocyte-derived macrophages, possibly in LpM form, are "antiendometriosis." These observations highlight the importance of monocyte-derived macrophages in limiting disease progression.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | MOUSE MODEL; CAVITY MACROPHAGES; TISSUE; MONOCYTES; INSIGHTS; LESIONS; GROWTH; CELLS; lesion; phenotype; ontogeny |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 16 Sep 2022 06:49 |
| Last Modified: | 16 Sep 2022 06:49 |
| URI: | https://pred.uni-regensburg.de/id/eprint/47512 |
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