Background & Aims

Inflammatory pain causes an increased response to noxious stimuli or pain due to normally innocuous stimuli. To better understand the mechanisms underlying hyperalgesia, it is essential to develop practical and relevant models of inflammation. In contrast to the large number of animal models, only a few studies have looked at human models that reflect bacterial inflammation.

Methods

To induce inflammation in human skin, lipopolysaccharide (LPS) was injected intradermally into the volar forearms of healthy volunteers. To study the time course of inflammation, LPS was injected at intervals of 50-1.5 hours before blood flow and sensitivity to noxious stimuli were assessed. Mechanical force, heat and injection of an increasingly acidic solution were applied to inflamed or non-inflamed control sites. Volunteers periodically rated the perceived pain during the injection using a numerical rating scale.

Results

Injection of LPS resulted in localised inflammation, as indicated by increased blood flow and increased pain sensitivity to mechanical and acidic stimuli. Hyperemia peaked at 4.5 hours. Maximum pain hypersensitivity was observed at 4.5 – 6 hours and had largely resolved by 50 hours after LPS injection.

Conclusions

This model of skin inflammation reliably induces hyperalgesia in human skin. The model can therefore be used to test substances that interfere with the development of inflammation and inflammatory pain.

References

Buters et al., Br J Clin Pharmacol. 2022; 88:680-690 (doi: 10.1111/bcp.14999)
Basran et al., J Leukoc Biol. 2013; 93:7-19 (doi: 10.1189/jlb.0512250)

Presenting Author

Felix Resch

Poster Authors

Michael Fischer

M.D., Ph.D.

Medical University of Vienna

Lead Author

Felix Jakob Resch

Medical University of Vienna

Lead Author

Stefan Heber

Medical University of Vienna

Lead Author

Topics

  • Models: Acute Pain