Inflammation Changes the Nervous System’s Response to Pain

A new study from researchers at the National Institutes of Health (NIH) offers insights into how the nervous system converts physical stimuli, such as heat and touch, into sensory signals and how inflammation alters these signals to promote pain. Conducted in mice, the study focuses on the specialized nerve cells known as somatosensory neurons, which detect tactile and thermal information from the skin and transmit it to the brain.

Different neurons process heat and touch

Using a combination of molecular profiling and real-time imaging techniques, the researchers analyzed how somatosensory neurons respond to distinct stimuli. Their results showed that separate groups of neurons are responsible for detecting gentle heat and light touch. However, when these stimuli became more intense, neuron activity began to overlap, indicating a shared cellular response to potential tissue-damaging stimuli.

This convergence may help explain how the nervous system differentiates between innocuous and harmful sensations, and why higher intensities of heat or pressure can result in pain.

How inflammation alters sensory signaling

To examine how inflammation influences these processes, the researchers introduced prostaglandin E2, a molecule known to trigger inflammation, into the skin of mice. This induced a sensitized state in specific sensory neurons known as nociceptors, which became increasingly responsive to heat.

This heightened sensitivity persisted for an extended period, providing a mechanistic explanation for why heat often becomes more painful during inflammation. In contrast, the detection of gentle touch remained unchanged, suggesting that different signaling mechanisms are involved.

However, the study also observed that when nociceptors are chronically activated by inflammation, they may contribute to a phenomenon known as tactile allodynia – where normal touch sensations become painful. This was found to be consistent with prior findings implicating the ion channel PIEZO2 in this process.

Implications for pain treatment strategies

These findings are part of a broader effort by the collaborating teams of Drs. Alex Chesler and Nick Ryba at NIH to better understand the neural basis of sensation. Their work aims to uncover how sensory stimuli are processed by the nervous system and how changes in these processes contribute to chronic pain.

Though conducted in mice, the researchers emphasize the relevance of their findings to human biology. The mechanisms of sensory processing in mice and humans share significant overlap, which supports the potential translation of these insights into pain treatment strategies.

By mapping how different types of sensory neurons contribute to distinct pain experiences, the research paves the way for developing targeted therapies that address specific types of pain, such as inflammation-induced thermal or tactile pain.

Reference: Ghitani N, von Buchholtz LJ, MacDonald DI, et al. A distributed coding logic for thermosensation and inflammatory pain. Nature. 2025. doi: 10.1038/s41586-025-08875-6

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