Aims: 

To investigate the contribution of peripheral sensory and/or sympathetic nerves to the enhanced expression of ICAM-1 simultaneously with the increased recruitment of opioid peptide-containing leukocytes to promote the control of inflammatory pain.

Methods: 

Following animal care approval behavioral nociceptive testing was performed in Wistar rats with complete Freund's adjuvant (CFA) inflammation without or with degenerated peripheral sensory or sympathetic nerve fibers by their respective neurotoxins, capsaicin or 6-hydroxydopamine. The number of intercellular adhesion molecule-1 (ICAM-1) immunoreactive (IR) blood vessels and b-endorphin- (END-) or met-enkephalin- (ENK-)-containing leukocytes was examined by immunohistochemistry. The consequence of peripheral sensory or sympathetic nerve fibers elimination by their respective neurotoxins on endogenous opioid peptide-mediated peripheral analgesia was assessed in sensory neurons by behavioral nociceptive testing.

Results: 

Selective degeneration of peripheral sensory or sympathetic nerve fibers significantly abolished the enhanced expression of vascular endothelial ICAM-1 concomitant with the reduced subcutaneous immigration of END- and ENK-containing leukocytes during CFA rat hind paw inflammation. Consequently, the elimination of these nerve fibers abolished endogenous opioid peptide-mediated peripheral analgesia.

Conclusions: 

During localized inflammatory pain peripheral sensory and sympathetic nerve fibers augment the expression of vascular endothelial ICAM-1 simultaneously with the increased recruitment of opioid peptide-containing leukocytes which consequently promotes the endogenous opioid peptide-mediated inhibition of inflammatory pain. These support existing evidence about a close link between the nervous and the immune system.

Support: 

DFG grants MO 1006/1-4, SCHA 820/3-2, SCHA 820/4-1