Substance P and keratinocyte activation markers: An in vitro approach

Viac, J.; Guéniche, Audrey; Doutremepuich, Jean-Daniel; Reichert, Uwe; Claudy, A; Schmitt, Daniel

doi:10.1007/bf02505049

Cited by 46 publications

(28 citation statements)

References 28 publications

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“…In addition, SP has been shown to induce expression of endothelial leucocyte adhesion molecule (ELAM)-1 [47] and P-and E-selectin on human skin microvascular endothelium [40]. Furthermore, SP receptors have been identified on human skin keratinocytes, and incubation of these cells with SP induced expression of intercellular adhesion molecule (ICAM)-1 and production of cytokines, leading to keratinocyte activation [48]. As the parasite-macrophage interactions and the subsequent entry of the parasites into their target cells constitute the initial steps in the establishment of the disease, the inhibitory effect of SP on macrophage migration towards L. major parasites might result in abrogation of this initial step in the disease process and hence give protection to the host.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Leishmania major Promastigote‐Induced Macrophage Migration is Modulated by Sensory and Autonomic Neuropeptides

et al. 1998

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Ahmed AA, Wahbi A, Nordlind K, Kharazmi A, Sundqvist K-G, Mutt V, Lidén S. In Vitro Leishmania major Promastigote-Induced Macrophage Migration is Modulated by Sensory and Autonomic Neuropeptides. Scand J Immunol 1998;48:79-85 Recruitment, migration and adherence of macrophages and their interaction with inoculated promastigotes are key steps in the initiation of the inflammatory process in cutaneous leishmaniasis. Parasite-and nervous system-derived factors might be involved in this process. In the present study the chemotactic activities of live, killed and sonicated Leishmania major promastigotes and of the promastigote culture supernatant as well as the L. major surface protease gp63 towards a murine macrophage cell line, Raw 264.7, were investigated, using the Boyden technique. The sensory neuropeptides SOM, CGRP and SP, and the autonomic neuropeptides VIP and NPY, were also investigated for possible modulatory effects on this chemotaxis, using the living promastigotes. Living promastigotes were the most efficient attractants for macrophages compared with other forms of the parasites. Prior incubation of the macrophages with the parasites completely abolished the chemotactic activity. This might indicate that the living promastigote chemotaxis is a receptor-mediated process. On the other hand, paraformaldehyde-killed promastigotes not only failed to induce macrophage chemotaxis but also inhibited it in comparison with the control. The surface protease gp63 tended to inhibit the macrophage chemotactic activity and the sonicate tended to stimulate it compared with controls. The culture supernatant had no effect, indicating that the chemoattractive factors putatively synthesized by the living promastigotes are not released to the surrounding medium. Somatostatin inhibited L. major promastigoteinduced macrophage migration at a high concentration, 10 ¹6 M, while substance P inhibited it at both low concentrations, 10 ¹10 and 10 ¹9 M, and a high one, 10 ¹6 M, the last-mentioned having the greatest inhibitory effect. A stimulatory effect of calcitonin gene-related peptide was found at high concentrations, 10 ¹5 and 10 ¹6 M. Vasoactive intestinal peptide stimulated macrophage chemotactic activity at both a high, 10 ¹5 M, and at a low, 10 ¹9 M, concentration, the same concentration at which neuropeptide Y exerted its maximum inhibitory effect.

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Section: Discussionmentioning

confidence: 99%

In Vitro Leishmania major Promastigote‐Induced Macrophage Migration is Modulated by Sensory and Autonomic Neuropeptides

et al. 1998

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“…For example, production of the proinflammatory cytokines IL-1␣, IL-1␤, and IL-8 as well as the IL-1 receptor antagonist in murine and human keratinocytes is upregulated by SP (118,780,903). SP is capable of directly activating both murine and normal human keratinocytes to induce IL-1 in a dose-dependent manner (23,780,831), suggesting a regulatory role of sensory nerve fibers that extend directly into the epidermis where they come in direct contact with both keratinocytes and Langerhans cells (181,348).…”

Section: Tachykinins and Neurokinin Receptorsmentioning

confidence: 99%

“…Keratinocytes themselves have been reported to express preprotachykinin A mRNA and SP, indicating an autocrine induction of SP in human keratinocytes (37). Finally, SP may modulate cutaneous inflammatory responses by upregulation of cell adhesion molecule expression on keratinocytes (903).…”

Section: Tachykinins and Neurokinin Receptorsmentioning

confidence: 99%

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

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

546

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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“…It is likely that incision releases ET-1 into the skin, initially from keratinocytes, from where it acts on cutaneous nociceptors to both lower the threshold for tactile stimulation (Balonov et al, 2006) and to induce spontaneous impulses, leading to the central sensitization that underlies secondary hyperesthesia (LaMotte, 1992;Treede et al, 1992). Activation of cutaneous terminals of nociceptors also results in local release of glutamate and neuropeptides Substance P and CGRP (deGroot et al, 2000;Jin et al, 2006;McGovern et al, 1995), which can further stimulate keratinocytes (Viac et al, 1996) and lead to further release of ET-1.…”

Section: Discussionmentioning

confidence: 99%

Cutaneous endothelin-A receptors elevate post-incisional pain

Mujenda

Duarte

Reilly

et al. 2007

Pain

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The contribution of endothelin-1 (ET-1), acting via endothelin-A receptors (ET A ), on post-incisional pain was examined in a rat model of incision through the hairy skin of the lumbar dorsum. Postincisional mechanical hyperesthesia was evaluated by cutaneous trunci muscle reflexes (CTMR) of subcutaneous muscles responding to stimulation with von Frey filaments near the wound (primary responses) and at a distance, especially on the contralateral dorsum (secondary responses, involving spinal circuits). The role of ET A was determined by pre-incisional, subcutaneous injection of the selective receptor antagonist BQ-123 at the incision site, 15 min or 24 hr before surgery. Control incisions showed both primary tactile allodynia and hyperalgesia, and a weaker secondary hyperesthesia, peaking 3-4 h after surgery and lasting at least 24h. Primary allodynia, but not hyperalgesia, was dose-dependently suppressed by 15 min pre-incisional BQ-123. In contrast, both secondary allodynia and hyperalgesia were inhibited by local BQ-123. The suppression of primary allodynia by local antagonist disappeared in 24 h, but that of secondary hyperesthesia remained strong for at least 24 h. Systemically delivered BQ-123 was without effect on any post-incisional hyperesthesia, and if the antagonist was locally injected 24 h before surgery there was no difference on hyperesthesia compared to vehicle injected at that time. We conclude that ET-1, released from skin by incision, activates nociceptors to cause primary allodynia and to sensitize spinal circuits through central sensitization. Blockade of ET A in the immediate peri-operative period prevents the later development of central sensitization.

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Substance P and keratinocyte activation markers: An in vitro approach

Cited by 46 publications

References 28 publications

In Vitro Leishmania major Promastigote‐Induced Macrophage Migration is Modulated by Sensory and Autonomic Neuropeptides

In Vitro Leishmania major Promastigote‐Induced Macrophage Migration is Modulated by Sensory and Autonomic Neuropeptides

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

Cutaneous endothelin-A receptors elevate post-incisional pain

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