Neuro-immune Interactions
Neuro-immune Interactions - Related Videos
04:02
Fluorescence Imaging of Neuro-Immune Dynamics Using a Skull Implant
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2025
Source: Bisht, K., et al. Precise brain mapping to perform repetitive in vivo imaging of neuro-immune dynamics in mice. J. Vis. Exp. (2020)This video demonstrates fluorescence imaging of neuro-immune dynamics in a transgenic mouse with a skull implant. Vascular and neuronal stability is imaged alongside dynamic microglial changes, reflecting immune responses to neuronal activity.
08:42
Whole-mount Confocal Microscopy for Adult Ear Skin: A Model System to Study Neuro-vascular Branching Morphogenesis and Immune Cell Distribution
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Cited by 12 •
2018
Here, we describe a high resolution whole-mount imaging method in the entire adult mouse ear skin, which enables us to visualize branching morphogenesis and patterning of peripheral nerves and blood vessels, as well as immune cell distribution.
07:31
Detection of Fluorescent Nanoparticle Interactions with Primary Immune Cell Subpopulations by Flow Cytometry
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Cited by 13 •
2014
Analysis of nanoparticle interaction with defined subpopulations of immune cells by flow cytometry.
08:17
Precise Brain Mapping to Perform Repetitive In Vivo Imaging of Neuro-Immune Dynamics in Mice
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Cited by 5 •
2020
This protocol describes a chronic cranial window implantation technique that can be used for longitudinal imaging of neuro-glio-vascular structures, interactions, and function in both healthy and diseased conditions. It serves as a complementary alternative to the transcranial imaging approach that, while often preferred, possesses some critical limitations.
09:44
Neuro-rehabilitation Approach for Sudden Sensorineural Hearing Loss
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Cited by 10 •
2016
This article reports the development of a neuro-rehabilitation approach, "constraint-induced sound therapy (CIST)" for sudden sensorineural hearing loss. The aim of CIST is to prevent maladaptive cortical reorganization by using an enriched acoustic environment. CIST represents a safe, easy, inexpensive, and effective approach to treat sudden sensorineural hearing loss.
FAQs
These signaling molecules provide several communication routes between neurons and immune cells. Cytokines and chemokines can convey immune activation, while neurotransmitters and neuropeptides allow neural signals to influence immune-cell behavior. Because these signals operate together, their combined activity can coordinate inflammation and tissue protection, rather than producing an isolated response from either system.
Sensory nerves detect local inflammatory changes and can transmit that information through reflex pathways. Those pathways may modify immune-cell activity at affected tissues, linking detection of danger with regulation of inflammation. This mechanism helps explain how neural sensing can influence protective responses while also contributing to symptoms associated with infection, including pain.
Neural signals can help control inflammation, but immune responses remain necessary for protection against pathogens. Studying their interaction therefore focuses on balance: reducing harmful or excessive inflammation without weakening protective immunity. This perspective connects local tissue responses with broader outcomes such as barrier defense, fever, systemic inflammation, and recovery after infection.
A useful investigation can compare communication through neurotransmitters, cytokines, chemokines, and neuropeptides, while also considering sensory-nerve activity and immune-cell responses. Relevant outcomes include inflammatory regulation, tissue protection, pain, fever, barrier defenses, systemic inflammation, and recovery. Examining these signals alongside outcomes helps connect molecular communication with infection-related physiological effects.
Infection-related neurological symptoms can be examined as possible consequences of communication between inflammatory signals and neural pathways. Researchers can relate immune-cell activity and inflammatory mediators to sensory-nerve detection and resulting symptoms such as pain or fever. This approach may distinguish effects associated with host responses from broader consequences of pathogen-driven inflammation.
The main therapeutic relevance is identifying ways to regulate damaging inflammation while preserving immune protection. Findings about neural signals, immune mediators, and reflex pathways could reveal points where excessive inflammatory activity can be moderated. Such work is especially relevant when infection produces systemic inflammation or neurological symptoms, because treatment must avoid compromising defenses against the pathogen.