Mast Cells in Cluster Headache. Ultrastructure, Release Pattern and Possible Pathogenetic Significance

P, Liberski; Mirecka, B

doi:10.1046/j.1468-2982.1984.0402101.x

Cited by 17 publications

(5 citation statements)

References 14 publications

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“…Mast cells are in a close spatial relationship to nociceptive fibers (8,9) and they release different mediators upon stimulation by neurotransmitters (10,11). Of interest, mast cells have been described more numerous in the painful area of patients with CH, in close proximity to trigeminal nerve endings (12)(13)(14). To date, the involvement of CGRP and/or mast cells in CH attacks induced by either PACAP38 or VIP has never been investigated.…”

Section: Introductionmentioning

confidence: 99%

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

et al. 2021

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Background Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide can provoke cluster headache attacks in up to half of cluster headache patients in their active phase. At present, it is unknown whether provoked attacks are mediated via calcitonin gene-related peptide or mast cell activation. Methods All enrolled patients with cluster headache were randomly allocated to receive a continuous infusion of either PACAP38 (10 pmol/kg/min) or vasoactive intestinal polypeptide (8 pmol/kg/min) over 20 min. We collected clinical data and measured plasma levels of calcitonin gene-related peptide and markers of mast cell activation (tryptase and histamine) at fixed time points: at baseline (T0), at the end of the infusion (T20), 10 min after the infusion (T30), and 70 min after the infusion (T90). Results Blood was collected from episodic cluster headache patients in active phase (n = 14), episodic cluster headache patients in remission (n = 15), and chronic cluster headache patients (n = 15). At baseline, plasma levels of calcitonin gene-related peptide, tryptase, and histamine were not different among the three study groups. Plasma levels of calcitonin gene-related peptide ( p = 0.7074), tryptase ( p = 0.6673), or histamine ( p = 0.4792) remained unchanged during provoked attacks compared to attack-free patients. Conclusion Cluster headache attacks provoked by either PACAP38 or vasoactive intestinal polypeptide were not accompanied by alterations of plasma calcitonin gene-related peptide, tryptase or histamine. The provoked attacks may not be mediated by calcitonin gene-related peptide or mast cell activation. Trial Registration: The study is registered at ClinicalTrials.gov (NCT03814226).

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Section: Introductionmentioning

confidence: 99%

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

et al. 2021

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“…disorders [6,56,57], while estrogens have been shown to affect immune responses [13] and mast cell secretion [47][48][49][50], For instance, mast cells arc thought to participate in the pathophysiology of vascular headaches [10,54], which are more frequent in women than in men and which may also be associated with food allergy [58,59], Other neuroimmunoendocrine diseases, such as multiple sclero sis, have also been associated with mast cells [11], occur more frequently in females [60,61], and multiple sclerosis patients also have a higher incidence of migraine head aches [62]. Increased numbers of mast cells have also been found in the painful bladder disorder interstitial cystitis [9], as well as in urticaria and angioedema [63], both of which occur more frequently in women.…”

Section: Discussionmentioning

confidence: 99%

“…Mast cells have been known mainly for their involve ment in allergic reactions [1], where they secrete many bi ologically important chemicals in response to immunoglo close apposition to neurons [7], prompting the suggestion that mast cell activation may participate in certain inflam matory conditions [6,8], such as irritable bowel disease [8], interstitial cystitis [9), vascular headaches [10] and possibly multiple sclerosis [11], The prevalence of these syndromes is higher in women, pointing to the involvement of sex hor mones. In fact, female sex hormones arc implicated in the regulation of the immune system [12,13], and sometimes exacerbate both allergies [14] and asthma [15,16].…”

Section: Introductionmentioning

confidence: 99%

Estradiol Augments while Tamoxifen Inhibits Rat Mast Cell Secretion

Vliagoftis

Dimitriadou

Boucher

et al. 1992

Int Arch Allergy Immunol

151

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Mast cells have been studied extensively for their involvement in allergic reactions, where they secrete numerous powerful mediators in response to immunoglobulin E and specific antigens. However, they are also triggered by neuropeptides, they have been found in close contact with neurons, and they are activated in diseases such as angioedema, interstitial cystitis and irritable bowel disease, the prevalence of which is much higher in women. When tested on purified rat peritoneal mast cells, 17β-estradiol augmented secretion of histamine and serotonin, starting at 1 μM and in a dose-dependent manner, whether stimulated by the mast cell secretagogue compound 48/80 or the neuropeptide substance P. However, 17β-estradiol did not augment mast cell secretion stimulated by immunoglobulin E and specific antiserum indicating that immunologic stimulation is under different regulation. Testosterone inhibited secretion induced by compound 48/80. Tamoxifen, an estrogen receptor antagonist used in the treatment of breast cancer, inhibited serotonin and histamine release from purified rat peritoneal mast cells triggered by compound 48/80 or substance P. Tamoxifen also inhibited the increase in intracellular free Ca²⁺ originating from an influx of extracellular Ca²⁺ in response to compound 48/80. Moreover, tamoxifen antagonized the synergistic effect of phorbol myristate and the cation ionophore A23187 on mast cell secretion, suggesting that tamoxifen’s inhibition may be due to regulation of protein kinase C activity. Tamoxifen may, therefore, have a beneficial effect in other neuroimmunoendocrine disorders both through estrogen receptor blockade and inhibition of mast cell secretion.

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“…Although it would be difficult to investigate intracranial mast cell populations in cluster headache patients, mast cells in skin biopsies taken from the temples show signs of increased degranulation (56–58). It is interesting to note that sympathetic vasoconstrictor activity suppresses neurogenic vasodilation (59), and that catecholamines inhibit mast cell degranulation (60); thus, release of sympathetic vasoconstrictor tone in patients with cervical sympathetic deficit could enhance vasodilation and promote the release of mast cell products.…”

Section: Possible Mechanisms Of Autonomic Disturbance In Cluster Headmentioning

confidence: 99%

Mechanisms of Autonomic Disturbance in the Face During and Between Attacks of Cluster Headache

Drummond

2006

Cephalalgia

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Drummond PD. Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache. Cephalalgia 2006; 26:633-641. London. ISSN 0333-1024 Lacrimation and nasal secretion during attacks of cluster headache appear to be due to massive trigeminal-parasympathetic discharge. In addition, the presence of oculo-sympathetic deficit and loss of thermoregulatory sweating and flushing on the symptomatic side of the forehead indicate that the cervical sympathetic pathway to the face is injured in a subgroup of cluster headache patients. In this review, it is argued that a peripheral rather than a central lesion produces signs of cervical sympathetic deficit, probably resulting from compression of the sympathetic plexus around the internal carotid artery. Although trigeminal-parasympathetic discharge appears to be the main trigger for vasodilation during attacks, supersensitivity to neurotransmitters such as vasoactive intestinal polypeptide, together with release of sympathetic vasoconstrictor tone, may boost facial blood flow in patients with cervical sympathetic deficit. In addition, parasympathetic neural discharge may provoke aberrant facial sweating during attacks in patients with cervical sympathetic deficit. Although neither trigeminal-parasympathetic discharge nor cervical sympathetic deficit appears to be the primary trigger for attacks of cluster headache, these autonomic disturbances could contribute to the rapid escalation of pain once the attack begins. For example, a pericarotid inflammatory process that excites trigeminal nociceptors might initiate neurogenic inflammation and trigeminal-parasympathetic vasodilation. To complete the loop, neurogenic inflammation and trigeminal-parasympathetic vasodilation could provoke the release of mast cell products, which aggravate inflammation and intensify trigeminal discharge. ᮀ Cluster headache, parasympathetic, sympathetic, vasoactive intestinal polypeptide

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Mast Cells in Cluster Headache. Ultrastructure, Release Pattern and Possible Pathogenetic Significance

Cited by 17 publications

References 14 publications

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation

Estradiol Augments while Tamoxifen Inhibits Rat Mast Cell Secretion

Mechanisms of Autonomic Disturbance in the Face During and Between Attacks of Cluster Headache

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