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ECZEMA IMMUNOPATHOGENSIS The immunopathogenesis of atopic eczema involves decreased cutaneous mediated immunity (Bos et al.). While not fully understood, substance P (SP) and C nerve fibers are implicated in pruitoceptive itch and nociceptive pain. Eczematous lesions expose C nerve fibers creating a pathway for reaction to the application of topical products. Through cell-learning, these reactions subside allowing for continuation of topical treatments involved in reduction symptoms and lesional activity. This paper will elucidate C nerve fiber and SP involvement. Pruritoceptive itch and nociceptive pain have been shown to be caused by the activation of very small nonmyelinated C nerve endings from large A? and A? myelinated nerve fibers. The C fiber?s free nerve endings are located near the dermoepidermal junction and are conducted centripetally by afferent nerves entering the spinal cord through the dorsal roots. Some research has shown that the eyelash growth itch responses is elicited in the C fiber nerve endings located in the epidermis, while the pain response is elicited in the dermal C fiber endings (Bigliardi-Qi et al.). Once activated, the primary neurons of the C fibers synapse to secondary neurons whose axons cross via the tractus spinothalamicus and arrive at the laminar nuclei of the thalamus. Finally, the laminar nuclei relay the signal to the cerebral cortex. The primary afferent neurons of C fibers have low conduction velocities of approximately 0.5 m/s and extend across innervation territories measuring up to 85 mm in the lower leg (Schmelz et al.). SP is a proinflammatory neuropeptide produced in dorsal ganglia and transported to periphery via A? and C nerve fibers. SP is from a group of neuropeptides called the tachykinins, which also include neurokinin A (NKA) and neurokinin B (NKB). SP is abundant in pruitoceptive C bibers and can release histamine from mast cell granules and provoke itch.