Mechanical but not painful electrical stimuli trigger TNF alpha release in human skin

Inflammatory consequences of cutaneous stimulation

“…Thus, the net result following nociceptor activation might depend on the relative concentrations of proinflammatory neuropeptides, such as substance P, and anti-inflammatory neuropeptides like CGRP. In human skin, a predominance of CGRP secreted from the peripheral terminals of nociceptive neurons during axon-reflex flares (Sauerstein et al, 2000) may explain why TNF-α did not increase following intradermal electrical stimulation in the study by Eberle et al (2010). It would be interesting to determine whether electrical stimulation is more effective in inflammatory and neuropathic pain syndromes characterized by heightened TNF-α signaling, because confirmation of a vicious circle between substance P and cytokine release could lead to insights about the pathogenesis of these syndromes.…”

“…In the meantime, the findings of Eberle et al (2010) indicate that innocuous mechanical stimulation of healthy skin is sufficient to raise intradermal levels of TNF-α, independent of activity in cutaneous nociceptive neurons. Cutaneous nerves might be more influential in the context of inflammation or nerve injury, due to sensitization of primary nociceptive afferents and up-regulation of TNF-α and other inflammatory mediators produced by resident skin cells Kress, 2004 andSabsovich et al, 2008).…”

“…The second intriguing observation by Eberle et al (2010) was the increase in levels of TNF-α in the dermal interstitial fluid 1 h after the train of impact stimuli. Inflammatory responses generally evolve over a period of hours or days rather than minutes because it takes time to manufacture cytokines.…”

“…Cutaneous nerves might be more influential in the context of inflammation or nerve injury, due to sensitization of primary nociceptive afferents and up-regulation of TNF-α and other inflammatory mediators produced by resident skin cells Kress, 2004 andSabsovich et al, 2008). In any event, the findings of Eberle et al (2010) suggest that even minor mechanical stimulation of affected regions may be sufficient to maintain inflammation and pain in patients with chronic neuro-inflammatory disease. If so, blocking the inflammatory response ought to be given priority over physical treatments that might inadvertently aggravate symptoms and cause the syndrome to persist.…”

Crosstalk the Microdialysis in Scientific Research: from Principle to its Applications

“…In the recent years, there were many articles reported for the tumor necrosis factor(TNF-α), IL-1,IL-6,IL-8, prostaglandin (PG), iso-prostaglandin F(2)-IsoPs, histamine and other inflammatory cytokines [90][91][92][93][94] to carry out the MD sampling, so as could evaluate the local anti-inflammatory drug pharmacodynamics. Shinkai et al [95] using the croton oil to establish the rat skin inflammation model, after the MD probe was implanted in the subcutaneous, then given the felbinac patch, the MD sample drug concentration was measured, wherein the PGE-2 levels were measured, the results showed that croton oil significantly increased the subcutaneous PGE-2 levels, while providing 0.5% or 3.5% felbinac patch after 2~5 h, the PGE-2 levels were significantly decreased.…”