| First Author | Schloss MJ | Year | 2022 |
| Journal | Nat Immunol | Volume | 23 |
| Issue | 4 | Pages | 605-618 |
| PubMed ID | 35352063 | Mgi Jnum | J:325749 |
| Mgi Id | MGI:7264849 | Doi | 10.1038/s41590-022-01165-7 |
| Citation | Schloss MJ, et al. (2022) B lymphocyte-derived acetylcholine limits steady-state and emergency hematopoiesis. Nat Immunol 23(4):605-618 |
| abstractText | Autonomic nerves control organ function through the sympathetic and parasympathetic branches, which have opposite effects. In the bone marrow, sympathetic (adrenergic) nerves promote hematopoiesis; however, how parasympathetic (cholinergic) signals modulate hematopoiesis is unclear. Here, we show that B lymphocytes are an important source of acetylcholine, a neurotransmitter of the parasympathetic nervous system, which reduced hematopoiesis. Single-cell RNA sequencing identified nine clusters of cells that expressed the cholinergic alpha7 nicotinic receptor (Chrna7) in the bone marrow stem cell niche, including endothelial and mesenchymal stromal cells (MSCs). Deletion of B cell-derived acetylcholine resulted in the differential expression of various genes, including Cxcl12 in leptin receptor(+) (LepR(+)) stromal cells. Pharmacologic inhibition of acetylcholine signaling increased the systemic supply of inflammatory myeloid cells in mice and humans with cardiovascular disease. |
