Unraveling the Gut-Brain Axis: Frontiers in Post-Stroke GI Care

New preclinical data suggest that ischemic stroke provokes rapid disruptions in intestinal immunity. Investigators used an established focal ischemia mouse model and profiled small‑intestinal mucosal immune cells, gut histology, and the microbiome. The dominant immune signal was hyperactivation of IgA‑producing plasma cells in the intestinal mucosa, with downstream effects on commensals and host–microbe interactions that plausibly drive dysbiosis.

Increased IgA can change which bacterial taxa are bound and retained at the mucosal surface, and experimental absence of IgA limited the magnitude of microbiome perturbation after stroke. Functional shifts included taxa‑level changes consistent with reduced colonization resistance, and mucosal IgA hyperactivity may perturb barrier function via epithelial–microbe signaling and local inflammatory tone.

Overall, the data support an IgA→microbiota pathway that likely mediates a substantial portion of post‑stroke enteropathy in these models.

Complementary preclinical work implicates neuronal enzyme–mediated pathways in post‑injury visceral hypersensitivity. Studies report upregulation of pain‑associated enzymes in visceral afferents, increased behavioral readouts of visceral pain, and electrophysiologic and pharmacologic evidence of enhanced afferent excitability after stroke.

Interactions between sensitized enteric neurons and altered mucosal immunity—especially where IgA‑driven dysbiosis increases noxious microbial signaling—can amplify visceral hypersensitivity and symptom burden. These data position neuronal-immune cross‑talk as a dual pathway and a potential translational target.