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)