# Extrinsic Gut-Innervating Neurons as Regulators of Intestinal Microbiota Sensing and Response

> **NIH NIH F32** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2021 · $65,994

## Abstract

Title: Extrinsic Gut-Innervating Neurons as Regulators of Intestinal Microbiota Sensing and Response.
Project Summary/Abstract
The goal of this project is to investigate the mechanisms by which gut-innervating neurons sense microbial stimuli
(from commensals, pathobionts, and pathogens) to modulate intestinal homeostasis and immune responses.
Gut-innervating neurons (GINs) are part of the peripheral autonomic nervous system and regulate intestinal
functions including motility, secretion, and immune homeostasis. They can be classified as intrinsic (or neuronal
component of the Enteric Nervous System; ENS), with cell bodies within the intestine, and extrinsic, with cell
bodies in ganglia outside of the intestine such as neurons innervating the intestine from the vagus nodose ganglia
(NG; vagal nerve), dorsal root ganglia (DRG), or celiac ganglia/superior mesenteric ganglia (CG-SMG). The
afferent and efferent peripheral circuits are organized in a reflexive manner to regulate immune responses and
inflammation. Despite the longstanding evidence of GINs dysfunction associated with dysbiosis, dysmotility and
colitis, few if any approaches have investigated the crosstalk between the extrinsic GINs and the microbiota in
modulating immune responses, even though the composition of the microbiota has been implicated in influencing
diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis and multiple sclerosis (MS). To better
elucidate which extrinsic GINs are responsible for sensing the microbiota and modulate intestinal homeostasis
and immune responses, we will combine a series of molecular, imaging and genetic techniques. Intestinal
microbiota regulate the balance between pro-inflammatory T helper 1 (Th1) and Th17 cells and anti-inflammatory
Tregs in the gut. Under homeostatic conditions, intestinal microbiota-mediated Th17 cell responses are non-
inflammatory and host tissue-protective. However, in the context of immune challenge or loss of immunological
tolerance, intestinal microbiota can drive inflammatory Th17 cell responses that can contribute to inflammatory
disease. Using various models from my sponsoring lab, we propose to elucidate how extrinsic GINs sense
microbes in the gut and modulate both the epithelial barrier as well as immune responses. Understanding how
extrinsic GINs sense gut microbiota may provide insights into mechanisms of host susceptibility to intestinal
infection, as well as organ-specific autoimmune disease, including IBD and MS.

## Key facts

- **NIH application ID:** 10156964
- **Project number:** 1F32AI157505-01
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Zoila Areli Lopez Bujanda
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $65,994
- **Award type:** 1
- **Project period:** 2020-12-01 → 2023-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10156964

## Citation

> US National Institutes of Health, RePORTER application 10156964, Extrinsic Gut-Innervating Neurons as Regulators of Intestinal Microbiota Sensing and Response (1F32AI157505-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10156964. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*