Differential release of serotonin without comparable histamine under diverse conditions in the rat mast cell

Theoharides, Theoharis C.; Kops, Sandra Kraeuter; Bondy, Philip K.; Askenase, Philip W.

doi:10.1016/0006-2952(85)90675-6

Cited by 77 publications

(46 citation statements)

References 45 publications

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“…[25][26][27] RMCP-II is a 25-kd serine protease that is specifi-mast cell hyperplasia did not correlate with the onset or early stages of hepatic fibrosis. Although our methcally found in the exocytotic granules of rat mucosal 5p0c$$0013 03-19-96 00:55:33 hepa WBS: Hepatology…”

Section: Fig 3 Enumeration Of Hepatic Mast Cells Identified By Tolumentioning

confidence: 99%

Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis

et al. 1996

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Mast cells have been shown to play a role in manyMast cells are granulated immunocytes that are bechronic inflammatory and fibrotic disorders. However, lieved to play a role in fibrotic reactions in a variety of their possible contribution to the pathological changes diseases. Increased numbers of mast cells have been that occur in liver cirrhosis is unknown. To explore this, observed in the vicinity of fibrotic lesions in rheumatoid we examined whether changes in hepatic mast cell num-arthritis, 1 inflammatory bowel disease, 2,3 scleroderma, 4 ber and mediator content were associated with fibrotic and fibrotic disorders of the lung. In the series of experiments reported here, our broad objective was to study associations between hepatic Received May 25, 1995; accepted November 13, 1995. patic mast cells release mediators that could contribute MATERIALS AND METHODSCopyright ᭧ 1996 by the American Association for the Study of Liver Animals. Male Sprague Dawley rats (200-250 g) were obDiseases.

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Section: Fig 3 Enumeration Of Hepatic Mast Cells Identified By Tolumentioning

confidence: 99%

Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis

et al. 1996

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“…There are any number of concerns with this explanation. Firstly, there is major con troversy as to whether peritoneal mast cells are cap able of taking up histamine [26,27], Second, these authors contend that the specific serotonin uptake inhibitor fluoxetine [28] could permit differential release and quote a previous paper [23] as having also done so, while in that paper fluoxetine was reported not to permit differential release. Moreover, a newer specific serotonin uptake inhibitor, sertraline [29], also did not permit differential release [unpubl.…”

Section: Discussionmentioning

confidence: 92%

“…One report indicated inability to reproduce differential release with amitriptyline [22], but it was unfortunate that those authors did not attempt to duplicate any aspect of the previously published study [10]: they used a dif ferent concentration of amitriptyline and of C48/80, and they carried out the study in vivo rather than in vitro. It was later shown that the tricyclic piperidine histamine-1 receptor antagonist hydroxyzine, as well as the monoamine oxidase inhibitor pargyline, also permitted differential release [23].…”

Section: Discussionmentioning

confidence: 99%

Progesterone Triggers Selective Mast Cell Secretion of 5-Hydroxytryptamine

Vliagoftis

Dimitriadou

Theoharides³

1990

Int Arch Allergy Immunol

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Mast cells are involved in allergic reactions where they secrete numerous mediators in response to immunoglobulin E and antigen. However, they have recently been implicated in neuroinflammatory conditions with a higher prevalence in women, and there have been clinical reports of progesterone anaphylaxis. When tested on purified rat peritoneal mast cells, progesterone alone stimulated release only of 5-hydroxy-tryptamine (serotonin) in a dose- and time-dependent manner. Serotonin release by progesterone was exceptional because it was not accompanied by histamine release or degranulation and was either augmented or unaffected by drugs which inhibit secretion induced by the classic mast cell secretagogue, compound 48/80. These findings indicate that mast cells are capable of selective serotonin secretion, previously shown only after pretreatement with certain tricyclic drugs, and may be involved in neuroendocrine syndromes.

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“…The mixed serotonin and HI-receptor antagonist cyproheptadine could inhibit brain vascular permeability and reduced EAE, possibly due to its ability (similar to that of hydroxyzine) to inhibit mast cell secretion (39). Inhibition ofEAE was also reported by the experimental mast cell "stabilizer" picroximil.…”

Section: Discussionmentioning

confidence: 93%

A Pilot, Open Label, Clinical Trial Using Hydroxyzine in Multiple Sclerosis

Logothetis¹,

Mylonas²,

Baloyannis

et al. 2005

Int J Immunopathol Pharmacol

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Multiple sclerosis (MS) is an autoimmune disorder of myelin destruction. Blood-brain-barrier (BBB) disruption precedes pathological or clinical findings and could involve mediators from perivascular brain mast cells, such as histamine and vascular endothelial growth factor (VEGF). Mast cells could be activated by many triggers, including acute stress that has been correlated with MS exacerbations. We considered that the histamine-1 (HI) receptor antagonist hydroxyzine, which also partially inhibits brain mast cells and has anxiolytic properties, may reduce MS symptoms. This open label, pilot, clinical trial investigated the effect on MS of an oral solution of hydroxyzine (100 mg per day), together with caffeine (200 mg per day) to reduce sedation. Twenty patients (8 males; 12 females) with relapsing-remitting or relapsing-progressive MS completed the study (12 ± 1 months) and were evaluated using disability scales. Most patients on hydroxyzine (75%) remained stable or improved neurologically and all but one showed improved mood. Hydroxyzine could be used as an adjuvant in MS, but the small number of patients enrolled and the short duration of the study precludes any definitive conclusions. A double-blind, placebo-controlled study is warranted.Multiple sclerosis (MS) is a human demyelinating disease characterized by brain edema and perivascular infiltrates ("cuffing") of mononuclear cells accompanied by various degrees of neurologic disability (1-2). Affected areas fill with fibrotic tissue forming the MS plaques that also contain activated mast cells (3). Blood-brain-barrier (BBB) breakdown precedes any pathological or clinical signs of MS (4-5). Acute stress can disrupt the BBB in rats (6). Most recently, acute stress was shown to increase BBB permeability to 99 Technetium-g1uceptatethrough the involvement ofbrain mast cells (7) and corticotropinreleasing-hormone (eRR) (7). It is, therefore, of interest that MS symptoms can be precipitated by psychological stress (8-9); a meta analysis and two recent publications confirmed a correlation between stress and MS attacks (10).Mast cells are typically activated by 19E and specific antigen in allergic reactions, as well as in innate and acquired (11) immunity. They have also been increasingly implicated in neuroinflammatory conditions, especially those worsened by stress (12). Mast cells have been associated with brain demyelination (13)(14) and are activated in

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Differential release of serotonin without comparable histamine under diverse conditions in the rat mast cell

Cited by 77 publications

References 45 publications

Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis

Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis

Progesterone Triggers Selective Mast Cell Secretion of 5-Hydroxytryptamine

A Pilot, Open Label, Clinical Trial Using Hydroxyzine in Multiple Sclerosis

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