GI Motility: Microbiota and Macrophages Join Forces

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GI Motility: Microbiota and Macrophages Join Forces Michelle L. Robinette, Marco Colonna Cell Volume 158, Issue 2, Pages 239-240 (July 2014) DOI: 10.1016/j.cell.2014.06.040 Copyright © 2014 Elsevier Inc. Terms and Conditions

Figure 1 A Model for Neuroimmune Crosstalk Regulating GI Tract Peristalsis The presence of bacterial products, including LPS, causes enteric neurons to produce CSF1, which binds to the CSF-1R on CX3CR1+CD11cloMHCIIhi MMs and promotes their maintenance. MMs produce BMP2, which binds to the BMP receptor, composed of BMPRI and BMPRII, the latter of which is expressed on axons in the myenteric plexus, but not in ICC or enteric glia. Through a yet-undefined mechanism, BMP2 binding to enteric neurons regulates intestinal motility. Submucosal neural plexus and additional ICC layers are excluded for simplicity. Cell 2014 158, 239-240DOI: (10.1016/j.cell.2014.06.040) Copyright © 2014 Elsevier Inc. Terms and Conditions