Abstract
Inflammation arising from the summation of the various effects of stimulation of peripheral nerves is referred to as neurogenic inflammation. The hallmark of neurogenic inflammation is increased vascular permeability due to activation of neurokinin 1 (NK1) receptors located on postcapillary venules by substance P (SP) released from sensory nerve fibers.133 This effect is transient, and participation of sensory nerves in both acute and chronic inflammation is the result of subsequent activation of cells of the immune system (particularly mast cells) and continued stimulation of release of inflammatory mediators or neuropeptides. This process has been reported to affect a variety of organs, including the bladder, skin, gut, lungs, airways, eye, and joints.3,93,179,213 Antidromic stimulation of unmyelinated sensory C fibers results in plasma extravasation and accumulation of leukocytes in the bladder and other organs.91,114,157 Various stimuli, such as antigens, cold, heat, bacterial or viral infection, or direct stimulation of nerves can initiate neurogenic inflammation.93,179,213 The concept that sensory nerves participate in amplification of local inflammation is further substantiated by the observation that prolonged blockade of the sciatic nerve with a local anesthetic (bupivacaine) significantly decreased (but did not ablate) carrageenan-induced paw swelling in the rat.65 Often the effects of neurogenic inflammation remain long after the inciting cause is gone. The processes associated with neurogenic inflammation also play a significant role in the amplification of inflammation to a level that may be disproportionate to the original insult.21
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Bjorling, D.E., Beckman, M., Saban, R. (2003). Neurogenic Inflammation of the Bladder. In: Atala, A., Slade, D. (eds) Bladder Disease, Part A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-8889-8_37
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