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Related Experiment Video

Updated: May 16, 2026

Cutaneous Surgical Denervation: A Method for Testing the Requirement for Nerves in Mouse Models of Skin Disease

Cutaneous Surgical Denervation: A Method for Testing the Requirement for Nerves in Mouse Models of Skin Disease

Published on: June 26, 2016

Neuronal derivative mediators that regulate cutaneous inflammations.

Norihisa Mikami¹, So-Ichiro Fukada, Hiroshi Yamamoto

¹Laboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka University, Osaka, Japan.

Critical Reviews in Immunology

|December 15, 2012

Summary

This summary is machine-generated.

Neurotransmitters like CGRP and SP influence skin inflammation by interacting with immune cells. Their roles in allergic contact dermatitis and atopic dermatitis are complex and depend on Th1/Th2 immune responses.

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Area of Science:

Immunology
Neuroscience
Dermatology

Background:

Allergic skin diseases involve complex immune regulation by various mediators.
Neurotransmitters released from nerve endings modulate immune cell functions via G-protein coupled receptors.

Purpose of the Study:

To review the physiological roles of key neurotransmitters and prostaglandins in cutaneous immunity.
To examine their receptor signaling pathways and effects on Th1/Th2-mediated skin inflammation.

Main Methods:

Review of existing literature on neurotransmitter and prostaglandin interactions in skin inflammation models.
Analysis of signaling pathways including cAMP/PKA, PLC, and calcium ion channels.
Focus on studies involving contact hypersensitivity (CHS), allergic contact dermatitis (ACD), and atopic dermatitis (AD).

Main Results:

Neurotransmitters such as calcitonin gene-related peptide (CGRP), substance P (SP), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase-activating polypeptide (PACAP) interact with immune cells.
Prostaglandins (PGs) also play a role in cutaneous immunity.
Their precise physiological effects in allergic skin conditions are debated due to complex inflammatory mechanisms and differing Th1/Th2 responses.

Conclusions:

Neurotransmitters significantly influence the type of inflammatory cells and immune reactions in skin inflammation.
Understanding the distinct roles of these mediators in Th1- versus Th2-driven inflammation is crucial.
Further research is needed to elucidate the complex physiological roles of neurotransmitters in skin immunity.