Subhash Kulkarni

This study identifies immune-defined subtypes of gastrointestinal disease in systemic sclerosis using proteome-wide serology, revealing distinct autoantibody profiles and clinically meaningful disease phenotypes.

This study identifies a neuronal PCSK1-M-ENK pathway in the ENS that suppresses colorectal cancer growth through OGFr activation.

This study identifies reduced enteric Bdnf and altered VIPergic signaling as key mechanisms of GI dysmotility in a Mecp2-null mouse model of Rett syndrome.

This study develops a novel benzodiazepine, Li633, that targets peripheral GABAA receptors to reduce visceral pain in IBS and FD models.

This study identifies IBD type-associated EGC activation signatures and reveals TNF/IFN-γ-driven necroptosis of activated enteric glia in inflammatory bowel diseases.

The paper identifies that post-inflammatory GI dysmotility results from ENS remodeling driven by monocyte recruitment and neuroinflammation, which can be prevented by enhancing HIF1 signaling in enteric neurons.

The paper detects mitotic neuroblasts in adult murine and human small intestinal myenteric plexus, providing evidence of steady-state neurogenesis.

This paper optimizes immunohistochemical protocols for assessing the enteric nervous system in formalin-fixed human tissue using multiple protein markers.

This study shows stress-induced glucocorticoid signaling reduces BDNF-TrkB signaling in the enteric nervous system, leading to GI dysmotility, and identifies TrkB as a potential therapeutic target.

This study shows that age-related changes in the lineage composition of the enteric nervous system affect gut health, with mesoderm-derived neurons becoming dominant and functional effects on intestinal motility that can be reversed by GDNF.

COUNTEN is an AI tool that rapidly and objectively enumerates and classifies enteric neurons in murine ileal plexus tissue, improving upon manual methods by reducing time and bias.

This study shows that intestinal bacteria maintain adult enteric neurons via TLR2-induced neurogenesis in mice, with implications for treating colonic motility disorders.