Neuropeptides

Abstract

uccessful repair of injured tissues requires diverse interactions between cells, biochemical mediators, and the cellular microenvironment. [1][2][3] Much has been learned about the individual events that are involved in this process, but their integration is clearly far more complex than has been imagined, and the important role of neurogenic stimuli is only recently being recognized.Neurogenic stimuli profoundly affect cellular events that are involved in inflammation, proliferation, and matrix, as well as cytokine and growth factor synthesis. Immune cells regulated by neuropeptides include lymphocyte subsets, macrophages, and mast cells. In addition, neuropeptides may affect the proliferative and synthetic activity of epithelial, vascular, and connective tissue cells. Furthermore, a close interaction between the nervous and the immune systems has become obvious. 4 The peripheral nervous system (PNS), acting through neuropeptides, not only relays sensory information to the central nervous system (CNS) but also plays an effector role in the inflammatory, proliferative, and reparative processes after injury. These effects range from growth factor and cytokine responses to control of local blood flow. Neuropeptides mediate many of the actions important in tissue-nervous system communication.We review the accumulated knowledge about the role of neuropeptides in inflammation as it pertains to tissue repair. NEUROPEPTIDES OF THE PNSNeuropeptides constitute one of the largest families of extracellular messengers, having a long phylogenetic history. They can act as neurotransmitters, hormones, and paracrine factors.

Treatment with the NK1 Antagonist Emend Reduces Blood Brain Barrier Dysfunction and Edema Formation in an Experimental Model of Brain Tumors

“…The link between inflammation and cancer has been well established, with many chronic inflammatory states associated with cancer development, as inflammation increases both mitogenesis and mutagenesis [33] [15]. Similarly, it is well known that both SP and the NK1 receptor are increased in inflammatory conditions [34], with increased expression of SP and NK1 receptor mRNA reported in response to inflammation [35]. SP induces and augments many aspects of the inflammatory response, including leukocyte activation, endothelial cell adhesion molecule expression, cytokine production and mast cell activation [36] [37].…”

Morphine-induced early delays in wound closure: Involvement of sensory neuropeptides and modification of neurokinin receptor expression

“…Neuropeptides peripherally released by primary afferent neurons following injury are essential for mediating the early components of neurogenic inflammation and initiating the healing process [62]. While other neuropeptides (e.g.…”

A neurokinin 1 receptor antagonist decreases postoperative peritoneal adhesion formation and increases peritoneal fibrinolytic activity

“…SP is known to play an important role in inflammatory (22,23), proliferative (24), and wound healing (25) processes. Known SP effects range from increasing inflammatory cytokine mRNA expression and secretion (26) to stimulating angiogenesis (27) and proliferation of fibroblasts (28).…”