Human mast cell heterogeneity: Histamine release from mast cells dispersed from skin, lung, adenoids, tonsils, and colon in response to IgE-dependent and nonimmunologic stimuli

Ma, Lowman; Ph, Rees; Rc, Benyon; Mk, Church

doi:10.1016/0091-6749(88)90199-6

Cited by 248 publications

(136 citation statements)

References 41 publications

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“…Histamine releasing activity of peptides (Lowman et al, 1988). Histamine release The ability of substance P fragments SP2 11, SP311 and SP4-11 to release histamine from human skin mast cells was compared with that of substance P in 4-7 experiments ( divided into 3 sub-classes, NK-1, NK-2 and NK-3, stance P (>M) on the basis of relative potencies of eledoisin, physalaemin, neurokinin A and neurokinin B to cause contraction (Lee et al, 1986).…”

Section: Resultsmentioning

confidence: 99%

“…The similarity of this response to that for compound 48/80, poly-L-lysine and morphine, and inhibition of the response to each secretagogue by a substance P antagonist, suggest that they share a common pathway of activation-secretion coupling distinct from that of IgE-dependent activation. Human skin mast cells are distinct from other human mast cells so far studied in their ability to respond to basic, non-immunological stimuli (Lowman et al, 1988) and this may well reflect a specialized function for these cells. M.A.L.…”

Section: Discussionmentioning

confidence: 99%

“…In our studies of mast cells dispersed from human skin, lung, tonsils, colon and adenoids, we established that skin mast cells are unique amongst these in releasing histamine in response to compound 48/80, morphine and substance P (Benyon et al, 1987;Lowman et al, 1988). In this paper we extend our observations on the ability of neuropeptides to induce histamine release from human skin mast cells and suggest that they activate histamine release by binding via basic moieties to the same, or a closely related, binding site distinct from the IgE-receptor.…”

Section: Introductionmentioning

confidence: 99%

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Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

Lowman

Benyon

Church

1988

British J Pharmacology

199

103

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1 Human skin mast cells, unlike other human mast cells so far studied, released histamine in a concentration-related manner in response to substance P, vasoactive intestinal peptide (VIP) and somatostatin (1 yM to 30 yM). In contrast, eledoisin, physalaemin, neurokinin A, neurokinin B, calcitonin gene-related peptide (CGRP), neurotensin, bradykinin and Lys-bradykinin induced negligible histamine release. 2 The low histamine releasing activity of physalaemin, eledoisin, neurokinin A and neurokinin B relative to substance P suggests that the human skin mast cell activation site is distinct from the tachykinin NK-1, NK-2 or NK-3 receptors described in smooth muscle.3 The relative potencies of substance P and its fragments SP2 11, SP3 11, SP4_11 and SP1,4 in releasing histamine from human skin mast cells suggests that both the basic N-terminal amino acids and the lipophilic C-terminal portion of substance P are essential for activity. 4 Peptide-induced histamine release, like that induced by compound 48/80, morphine and poly-Llysine, is rapid, reaching completion in 10-20s, is largely independent of extracellular calcium but requires intact glycolysis and oxidative phosphorylation. The substance P analogue, [D-Pro4,D-Trp7'9 "0] SP411 (SPA), not only reduced substance Pinduced histamine release in a concentration-related manner but also inhibited that induced by VIP, somatostatin, compound 48/80, poly-L-lysine and morphine but not anti-IgE. 6 The similar characteristics of histamine release induced by substance P. VIP, somatostatin, compound 48/80, poly-L-lysine and morphine suggest that they share a common pathway of activationsecretion coupling distinct from that of IgE-dependent activation. Furthermore, the ability of human skin mast cells to respond to basic non-immunological stimuli including neuropeptides may reflect a specialised function for these cells.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

Lowman

Benyon

Church

1988

British J Pharmacology

199

103

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“…Human lung cells were dispersed from macroscopically normal human lung by an enzymatic procedure described previously (11). Mast cell numbers were counted in a Neubauer hemocytometer after metachromatic staining with Kimura stain (12).…”

Section: Purification and Culture Of Human Lung Mast Cellsmentioning

confidence: 99%

NF-κB and TNF-α: A Positive Autocrine Loop in Human Lung Mast Cells?

Coward

Okayama

Sagara

et al. 2002

The Journal of Immunology

123

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The generation of cytokines, particularly TNF-α, by mast cells is crucial for the initiation of the allergic response. A key transcription factor involved in the synthesis of TNF-α is NF-κB. Using a mAb specific for the activated form of NF-κB, immunocytochemistry, confocal microscopy, and gel shift assays have been used in conjunction to localize this transcription factor to human lung mast cells and to study its activation. Activation of mast cells with stem cell factor (10 ng/ml) and anti-IgE (1 μg/ml) induced maximal activation of NF-κB at 4 and 2 h, respectively. In contrast, with TNF-α (5 ng/ml) maximal activation occurred within 15 min. Parallel falls in IκB were demonstrated. Confocal microscopy demonstrated the localization of the activated form of NF-κB to the nuclei of activated mast cells. NF-κB activation was verified using a gel shift assay. A supershift assay showed mast cell NF-κB to be composed primarily of p50 with smaller amounts of p65. No interaction with Abs for Rel-A, c-Rel, Rel-B, and p52 was seen. Immunocytochemistry and ELISAs showed TNF-α to be stored within mast cells and released into the extracellular environment following activation. The possible participation of TNF-α generated by mast cells in NF-κB activation by anti-IgE was investigated using a blocking Ab for TNF-α. The blocking Ab reduced NF-κB activation by anti-IgE by >50%, suggesting that the release of preformed mast cell-associated TNF-α acts as a positive autocrine feedback signal to augment NF-κB activation and production of further cytokine, including GM-CSF and IL-8.

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“…Mast cells from normal human breast skin (from plastic surgery), or in the case of urticaria patients from 4-mm punch biopsies (uninvolved skin from the upper thorax, were isolated by enzymatic dispersion, with slight modification as described before (8). Briefly, skin was cut into small pieces (1-2 mm'), dispersed in two 1-11 cycles with collagenase and hyaluronidase ( 15 and 7.5 mg/g tissue, respectively, in 2.5 ml medium/g tissue), separated from undissociated tissue by filtration through nylon gauze ( 150 pm) and then washed twice in Pipes A.…”

Section: Preparation Of Human Skin Must Cellsmentioning

confidence: 99%

Histamine releasability of basophils and skin mast cells in chronic urticaria

Zuberbier

Schwarz

Hartmann

et al. 1996

Allergy

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The following reagents were purchased: Pipes, collagenase type la, hyaluronidase type I-S, N-FMLP, PAF (Sigma, Deisenhofen, Germany), anti-IgE (polyclonal from goat, Behring, Marburg, Germany), DNAse I (Boehringer, Mannheim, Germany), A23 187 (Calbiochem, Bad Soden, Germany), cimetidine (SmithKline Beecham, Munich, Germany), MEM/Earle's salts, FCS, IL-3 (Gibco, Berlin, Germany), histamine EIA (highly specific for histamine, sensitivity 0.2 nM; Immunotech, Hamburg, Germany), LTC, EIA (cross reaction with leukotriene (LT)D,: 46%, LTE,: 2% and LTB,: t0.01%, sensitivity 18 pg/ml, Cayman, Ann Arbor, MI, USA).Bufers. Pipes A (containing 0.1% HSA), Pipes EDTA (Pipes A containing 2% 0.1 M EDTA), and Pipes ACM (Pipes A containing 2 mM CaCI, and 0.5mM MgC1,) were used in all experiments at a pH of 7.40.Medium. In all experiments with mast cells, MEM containing 2% FCS, 1% penicillin and streptomycin, 1% glutamine, 2% MgSO,, and 10 pg/ml DNAse was used during the isolation process.

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Human mast cell heterogeneity: Histamine release from mast cells dispersed from skin, lung, adenoids, tonsils, and colon in response to IgE-dependent and nonimmunologic stimuli

Cited by 248 publications

References 41 publications

Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

Characterization of neuropeptide‐induced histamine release from human dispersed skin mast cells

NF-κB and TNF-α: A Positive Autocrine Loop in Human Lung Mast Cells?

Histamine releasability of basophils and skin mast cells in chronic urticaria

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