Increased compound 48/80 induced local histamine release from nonlesional skin of patients with chronic urticaria

Bédard, P.M.; Brunet, Chantal; Pelletier, G.; Hébert, Jacques

doi:10.1016/0091-6749(86)90260-5

Cited by 75 publications

(32 citation statements)

References 19 publications

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“…An augmenta tion of or defects in the interactions between neuropeptide-secreting neurones and skin mast cells may contribute to the aetiology of some forms of urticaria. The enhanced weal responses to various non-immunological stimuli observed in patients with chronic idiopathic urticaria [61,62] possibly suggest an in creased mast cell sensitivity as an underlying cause of this disease. …”

Section: Implications Of Mast Cell Activation By Neuropeptidesmentioning

confidence: 99%

Neuropeptide-Induced Secretion from Human Skin Mast Cells

Church

El-Lati

Caulfield

1991

Int Arch Allergy Immunol

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Unlike human mast cells associated with mucosal surfaces such as lung, adenoids, tonsils and intestine, skin mast cells may be stimulated to release histamine by the neuropeptides substance P, vaso-active intestinal polypeptide and somatostatin or by other basic secretagogues such as morphine and compound 48/80. Release of histamine by neuropeptides is rapid and accompanied by minimal generation of the eicosanoids prostaglandin D₂ and leukotriene C₄. Transient elevations of intracellular calcium are associated with mediator secretion induced by both immunological and non-immunological stimulation, that induced by anti-IgE being derived from extracellular sources through channels in the plasma membrane while that stimulated by neuropeptides is mobilized intracellulary. Similarly, elevations of intracellular cyclic AMP induced by anti-IgE occur only in the presence of extracellular calcium, whereas with substance P elevations are apparent even in the absence of extracellular calcium. With the latter stimulus, histamine release is complete before the peak cyclic AMP is achieved. Despite these biochemical and temporal differences, degranulation induced by both secretagogues proceeds by compound exocytosis which is indistinguishable under the electron microscope. From these results we suggest that IgE-dependent and neuropeptide stimulation of human skin mast cells proceed by distinct biochemical pathways which eventually merge to produce exocytosis of their preformed granule-associated mediators.

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Section: Implications Of Mast Cell Activation By Neuropeptidesmentioning

confidence: 99%

Neuropeptide-Induced Secretion from Human Skin Mast Cells

Church

El-Lati

Caulfield

1991

Int Arch Allergy Immunol

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“…Defects in neuropeptide/skin mast cell interactions may contribute to the aetiology of some forms of urticaria; enhanced wheal responses of patients with chronic idiopathic urticaria to various non-immunological stimuli have been noted [66,67], possibly suggesting increased mast cell sensitivity as an underlying cause of this disease. Clues to the nature of the skin mast cell stimulus in heat-and cold-induced urticaria may derive from pre vious comparisons of the levels of mast cell products in venous effluent of thermally challenged limbs; the high ratios of histamine to prostaglandin D2 (>1,000:1) [27,28] are suggestive of activation by non-immunological stimuli, possibly neuropeptides.…”

Section: Comparison Of Ige-dependent and Neuropeptide-induced Mediatomentioning

confidence: 99%

Interaction of Neuropeptides with Human Mast Cells

Robinson

et al. 1989

Int Arch Allergy Immunol

121

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Mast cells of human skin, but not lung, adenoids, tonsils, or intestine, release histamine in response to substance P, vasoactive intestinal polypeptide, and somatostatin. The substance P receptor of skin mast cells is not of the NK-1, NK-2 or NK-3 subtypes of smooth muscle. Time course and calcium dependency of release by peptides differed from anti-IgE. With anti-IgE, the molar ratios of histamine:PGD₂:LTC₄ generated by skin mast cells was 1,000:25:2, whereas with substance P these ratios were 1,000:1:0.1. Similar results were obtained with the other neuropeptides. The ability of peptides to stimulate skin mast cell histamine release suggests a mechanism whereby their release from dermal nerve endings is coupled to changes in micro-vasculature.

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“…An augmentation or de fects in the interactions between neuropep tide-secreting neurones and skin mast cells may contribute to the aetiology of some forms of urticaria. The enhanced weal re sponses to various non-immunological stim uli observed in patients with chronic idio pathic urticaria [63,64] possibly suggests an increased mast cell sensitivity as an underly ing cause of this disease.…”

Section: Discussionmentioning

confidence: 99%

Mediator Secretion from Human Skin Mast Cells Provoked by Immunological and Non-Immunological Stimulation

Church

Okayama

El-Lati³

1991

Skin Pharmacol Physiol

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Mast cells of the human skin not only release mediators following immunological activation, but may also be stimulated to release histamine by the neuropeptides substance P, vasoactive intestinal polypeptide and somatostatin or by other basic secretagogues such as morphine, poly-L-lysine and compound 48/80. Release of histamine under these conditions is rapid and accompanied by minimal generation of the eicosanoids, prostaglandin (PG)D₂ and leukotriene (LT)C₄. Transient elevations of intracellular calcium are associated with mediator secretion induced by both stimuli, that induced by anti-IgE being derived from extracellular sources through channels in the plasma membrane while that stimulated by neuropeptides is mobilized intracellularly. Similarly, elevations of intracellular cyclic adenosine monophosphate (AMP) induced by anti-IgE occur only in the presence of extracellular calcium whereas with substance P elevations are apparent even in the absence of extracellular calcium. With the latter stimulus, histamine release is complete before the peak cyclic AMP is achieved. Histamine release stimulated by both secretagogues is unaffected by sodium cromoglycate or nedocromil sodium but is reduced by both salbutamol and isobutylmethylxanthine. Despite these biochemical and temporal differences, degranulation induced by both secretagogues proceeds by compound exocytosis which is indistinguishable under the electron microscope.

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Increased compound 48/80 induced local histamine release from nonlesional skin of patients with chronic urticaria

Cited by 75 publications

References 19 publications

Neuropeptide-Induced Secretion from Human Skin Mast Cells

Neuropeptide-Induced Secretion from Human Skin Mast Cells

Interaction of Neuropeptides with Human Mast Cells

Mediator Secretion from Human Skin Mast Cells Provoked by Immunological and Non-Immunological Stimulation

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