Abstract
Noxious stimuli induce substance P (SP) secretion from nerve terminals, resulting in plasma extravasation, edema and hyperalgesia, commonly referred to as neurogenic inflammation. Since SP is a short-lived molecule, additional proinflammatory mediators maintain continued inflammation. The bladder contains stores of preformed macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, which is released into the lumen in response to SP. MIF may act in an amplifying manner to maintain or increase inflammation. Inducing inflammatory changes with SP, while sequestering released luminal MIF with an antibody, tested this hypothesis. In anesthetized rats the ureters were cut to isolate the bladder and the bladder contents were replaced with saline or antiMIF antibody (5 or 15 microg/ml), immediately followed by systemic SP or saline. Changes in the expression of inflammatory cytokines, and histological changes in the bladder and prostate were evaluated 1 hour later. : Targeted array analysis identified increases in proinflammatory gene expression in the bladder and prostate as a result of SP. SP induced changes in MIF, cyclooxygenase-2, nerve growth factor, c-fos and edema were decreased by intraluminal anti-MIF. SP incre...Continue Reading
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