Leonardo E. Navarro
Research Subjects
Leonardo E. Navarro has a total of 23 co-authors. Here are the top co-authors by number of shared publications:
- Amanda M. Clark
College of Pharmacy, Oregon State University 6 Department of Pharmaceutical Sciences Corvallis, OR
1 shared publication - Andrey Morgun
Oregon State University
1 shared publication - Azree Z. Ashraf
University of Massachusetts Chan Medical School 1 Department of Pathology Worcester, MA
1 shared publication - Balázs Koscsó
Department of Microbiology and Immunology, Penn State University College of Medicine and Milton Hershey Medical Center, Hershey, PA 17033, USA
1 shared publication - Changsik Shin
Penn State University College of Medicine 3 Department of Microbiology and Immunology Hershey, PA
1 shared publication - Chinmayee Dash
The Morningside Graduate School of Biomedical Sciences at the UMass Chan Medical School 5 , Worcester, MA
1 shared publication
Latest Publications
- 3 March 2026
- Published by Rockefeller University Press in Journal of Experimental Medicine
- Vol. 223 (4)
Inflammation rewires the enteric nervous system through neurogenic monocyte recruitment
Proper organization of the enteric nervous system (ENS) is critical for normal gastrointestinal (GI) physiology. Inflammatory bowel disease (IBD) disrupts key GI functions, including bowel motility. However, in many IBD patients, motility disorders persist even during remission, suggesting an irreversible ENS defect secondary to IBD. Here, we show that postinflammatory GI motility dysfunction arises from structural remodeling of the ENS, driven by a combination of neuronal loss and neurogenesis. During mucosal inflammation, enteric neurons upregulate CCL2 expression, facilitating the recruitment of monocytes into the myenteric plexus within the intestinal muscle. Monocyte-derived macrophages infiltrate the myenteric ganglia, contributing to excessive ENS remodeling and postinflammatory motility dysfunction. This neuroimmune axis is counterbalanced by a hypoxia-induced stress response in enteric neurons mediated by HIF1α. Enhancing the neuron-intrinsic hypoxia pathway limits ENS remodeling and preserves motility. In summary, this study presents a mechanistic model of postinflammatory GI motility dysfunction and proposes a therapeutic strategy to maintain ENS integrity and function during inflammation.
- 3 March 2026
- Published by Rockefeller University Press in Journal of Experimental Medicine
- Vol. 223 (4)
Inflammation rewires the enteric nervous system through neurogenic monocyte recruitment
Proper organization of the enteric nervous system (ENS) is critical for normal gastrointestinal (GI) physiology. Inflammatory bowel disease (IBD) disrupts key GI functions, including bowel motility. However, in many IBD patients, motility disorders persist even during remission, suggesting an irreversible ENS defect secondary to IBD. Here, we show that postinflammatory GI motility dysfunction arises from structural remodeling of the ENS, driven by a combination of neuronal loss and neurogenesis. During mucosal inflammation, enteric neurons upregulate CCL2 expression, facilitating the recruitment of monocytes into the myenteric plexus within the intestinal muscle. Monocyte-derived macrophages infiltrate the myenteric ganglia, contributing to excessive ENS remodeling and postinflammatory motility dysfunction. This neuroimmune axis is counterbalanced by a hypoxia-induced stress response in enteric neurons mediated by HIF1α. Enhancing the neuron-intrinsic hypoxia pathway limits ENS remodeling and preserves motility. In summary, this study presents a mechanistic model of postinflammatory GI motility dysfunction and proposes a therapeutic strategy to maintain ENS integrity and function during inflammation.