IRP study reveals how inflammation makes touch painful

Researchers uncover the cellular and molecular basis for sensing heat and inflammatory pain

Researchers at the National Institutes of Health (NIH) have discovered clues as to how our bodies turn sensations such as heat and touch into signals sent to the brain — and how these signals can be altered by inflammation to drive pain. The research focuses on the nerve cells in the skin that help us detect the location, intensity, and emotional quality of touch, known as somatosensory neurons. By combining advanced imaging techniques with detailed molecular analysis, the researchers explored how heat and touch activate different types of receptor cells in mice.

“To develop better treatments for pain, it’s critical that we deepen our understanding of the biology behind how sensory signals are received, transmitted, and ultimately perceived by the brain,” said Alex Chesler, Ph.D., co-author of the study and senior investigator at NIH. “Over the past few years, we developed a platform for watching sensation in action, revealing new details about the cells and molecules required and, in this study, how inflammation triggers pain.”

The research revealed how different types of cells were 'called into action' depending on whether the stimulus was innocuous, such as gentle warmth or touch, or noxious, meaning a stimulus strong enough to potentially cause damage to normal tissue. For example, heat and gentle touch were transmitted by entirely different types of cells. When the stimulus was more intense, the nerve cells began to overlap in their roles for transmitting the sensations of heat and pressure, providing an explanation for how cells detect and distinguish between innocuous and noxious stimuli.

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This page was last updated on Wednesday, April 23, 2025