# Unraveling transcriptomic and functional changes to immune sensing neuronal ganglia in response to allergy and bacteria

> **NIH NIH R21** · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · 2022 · $242,678

## Abstract

Project Summary
Allergies affect millions of Americans and are exacerbated by bacterial infection. Despite mainstay therapies that
suppress immune responses to allergy or bacteria, these health issues continue to persist. An unexplored target
for new therapies lies with neural surveillance and regulation of immunity. However, this neural influence is
poorly understood and seemingly paradoxical: immune responses are exacerbated in allergy, but in response to
bacterial infection, the neural response reduces inflammation. How might this happen?
One possibility is that the peripheral neural-immune sensing apparatus might be altered by such factors as
immunoglobulin profiles, and gender, implying the participation of sex hormones. We hypothesize that such
variables affect the transcriptome and thereby the excitability of the vagus and carotid bodies. Studies in AIM 1
will use single-cell RNAseq analysis of vagal and carotid body ganglia from male and female mice with asthma,
pneumonia to identify how these nerves are changed in response to each condition. Then, we will assess nerve
activity in response to immunoglobulin stimuli of each ganglia using state-of-the-art electrophysiological
recording techniques. This project will reveal which neural cluster (vagus vs. carotid body) is the predominant
sensory ganglia involved in regulating allergic vs. bacterial immune responses and how sex may affect neuro-
immune signalling. Studies in AIM 2 will utilize DTR (diphtheria toxin receptor) technology in mice to selectively
ablate cells where DTR expression is driven by TRPV1 (transient receptor potential vanilloid 1) or TH (tyrosine
hydroxylase). Use of these transgenic mice will allow ablation of either vagal (TRPV1-DTR) or carotid body (TH-
DTR) centers by direct neural microinjection of diphtheria toxin (DTX) into vagal or carotid body ganglia using
saline injections as control. We will then expose mice to either allergen or bacterial infections. DTX injections will
selectively abolish neuronal function and reveal which ganglion is the predominant neuro-immune sensor in the
specified condition in male and female mice.
These data will: 1) identify how the response to allergic or bacterial stimuli alters receptor gene expression in
order to identify the phenotypic switch from anti- to pro-inflammatory neural-immune signalling; 2) establish a
model and sex differences that will set the stage for further investigation involving targeted knockdown within
neuro-immune sensing ganglia to discern function; 3) validate our models and methods for future investigations
into the role of neural-immune sensing in disease states.

## Key facts

- **NIH application ID:** 10373360
- **Project number:** 1R21AI159221-01A1
- **Recipient organization:** LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER
- **Principal Investigator:** Nicholas Jendzjowsky
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $242,678
- **Award type:** 1
- **Project period:** 2022-05-06 → 2024-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10373360

## Citation

> US National Institutes of Health, RePORTER application 10373360, Unraveling transcriptomic and functional changes to immune sensing neuronal ganglia in response to allergy and bacteria (1R21AI159221-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10373360. Licensed CC0.

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