Role of Neutral Endopeptitidase (NEP) and Substance P in Cutaneous Inflammation: Increased Plasma Extravasation in NEP-Deficient Mice.

Steinhoff, Martin; Cholzen, T. S.; Luger, T A; Armstrong, Cheryl A.; Bunnett, N.W.; Ansel, J. C.

doi:10.1097/01206501-200103000-00040

Cited by 1 publication

(2 citation statements)

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“…In the skin, NEP (Ϫ/Ϫ) mice showed an increased constitutive plasma extravasation from postcapillary venules in several tissues including skin. Moreover, in a model of experimentally induced contact dermatitis of the ear, NEP (Ϫ/Ϫ) mice demonstrated a significant increase of plasma extravasation and cutaneous inflammation that peaked after 6 h (740,804). This leakage was attenuated by injection of recombinant NEP, or antagonists against NK1R and BK2-R, respectively.…”

Section: Agonist Removal By Neuropeptidedegrading Enzymesmentioning

confidence: 94%

“…Because afferent sensory neurons express specific receptors for neuropeptides, prostaglandins, histamine, neurotrophins, opioids, proteases, cytokines, and immunoglobulins (19), an interactive communication network between sensory nerves and immune cells likely exists during cutaneous inflammation (103,787). Finally, cell-associated neuropeptide-degrading peptidases such as neutral endopeptidase (NEP), angiotensin converting enzyme (ACE), or endothelin converting enzyme (ECE)-1 have been shown to modulate neurogenic inflammation by limiting the effects of neuropeptides in the skin (739,740,804). Thus the interaction between sensory nerves releasing neuropeptides, target cells with functional receptors, and neuropeptide-degrading peptidases is critical for determining neurogenic inflammation (Fig.…”

Section: A Towards a Modern Concept Of Neurogenic Inflammationmentioning

confidence: 99%

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Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

548

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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Section: Agonist Removal By Neuropeptidedegrading Enzymesmentioning

confidence: 94%