Substance P Induces the Expression of an Endothelial-Leukocyte Adhesion Molecule by Microvascular Endothelium

Matis, Wendy L.; Lavker, Robert M.; Murphy, Gëorge F.

doi:10.1111/1523-1747.ep12874665

Cited by 177 publications

(78 citation statements)

References 23 publications

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“…Moreover, it enhanced granulocyte infiltration into mouse skin both through degranulation of mast cells and by a direct action on endothelial cells [46]. 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].…”

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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“…• Substance P (Matis et al, 1990;Walsh et al, 1990a;Cocchiara et al, 1995) • Calcitonin gene-related peptide (Piotrowski and Foreman, 1986) Chemokines…”

Section: Selected Mast Cell Secretagoguesmentioning

confidence: 99%

Mast Cells and Oral Inflammation

Walsh

2003

Critical Reviews in Oral Biology & Medicine

152

114

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Mast cells are mobile granule-containing secretory cells that are distributed preferentially about the microvascular endothelium in oral mucosa and dental pulp. The enzyme profile of mast cells in oral tissues resembles that of skin, with most mast cells expressing the serine proteases tryptase and chymase. Mast cells in oral tissues contain the pro-inflammatory cytokine tumour necrosis factor-␣ in their granules, and release of this promotes leukocyte infiltration during evolving inflammation in several conditions, including lichen planus, gingivitis, pulpitis, and periapical inflammation, through induction of endothelial-leukocyte adhesion molecules. Mast cell synthesis and release of other mediators exerts potent immunoregulatory effects on other cell types, while several T-lymphocyte-derived cytokines influence mast cell migration and mediator release. Mast cell proteases may contribute to alterations in basement membranes in inflammation in the oral cavity, such as the disruptions that allow cytotoxic lymphocytes to enter the epithelium in oral lichen planus. A close relationship exists among mast cells, neural elements, and laminin, and this explains the preferential distribution of mast cells in tissues. Mast cells are responsive to neuropeptides and, through their interaction with neural elements, form a neural immune network with Langerhans cells in mucosal tissues. This facilitates mast cell degranulation in response to a range of immunological and non-immunological stimuli. Because mast cells play a pivotal role in inflammation, therapies that target mast cell functions could have value in the treatment of chronic inflammatory disorders in the oral cavity.

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“…The release of neuropeptides and other proinflammatory mediators by nerve terminals in the bladder could induce the initial plasma extravasation (Heller et al, 1994). These neuropeptides also induce increased expression of endothelial adhesion molecules (Matis et al, 1990;Hosoi et al, 1993). This in turn would attract circulating leukocytes, increased in number because of the systemic immune response to the virus, producing a positive feedback mechanism that aggravates the initial plasma extravasation.…”

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confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

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Substance P Induces the Expression of an Endothelial-Leukocyte Adhesion Molecule by Microvascular Endothelium

Cited by 177 publications

References 23 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

Mast Cells and Oral Inflammation

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

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