-
Allergology International : Official... Oct 2018Sweat allergy is defined as a type I hypersensitivity against the contents of sweat, and is specifically observed in patients with atopic dermatitis (AD) and cholinergic... (Review)
Review
Sweat allergy is defined as a type I hypersensitivity against the contents of sweat, and is specifically observed in patients with atopic dermatitis (AD) and cholinergic urticaria (CholU). The allergic reaction is clinically revealed by positive reactions in the intradermal skin test and the basophil histamine release assay by sweat. A major histamine-releasing antigen in sweat, MGL_1304, has been identified. MGL_1304 is produced at a size of 29 kDa by Malassezia (M.) globosa and secreted into sweat after being processed and converted into the mature form of 17 kDa. It induces significant histamine release from basophils of patients with AD and/or CholU with MGL_1304-specific IgE, which is detected in their sera. Patients with AD also show cross-reactivity to MGL_1304-homologs in Malassezia restricta and Malassezia sympodialis, but MGL_1304 does not share cross antigenicity with human intrinsic proteins. Malassezia or its components may penetrate the damaged epidermis of AD lesions and interact with the skin immune system, resulting in the sensitization and reaction to the fungal antigen. As well as the improvement of impaired barrier functions by topical interventions, approaches such as anti-microbial treatment, the induction of tolerance and antibody/substance neutralizing the sweat antigen may be beneficial for the patients with intractable AD or CholU due to sweat allergy. The identification of antigens other than MGL_1304 in sweat should be the scope for future studies, which may lead to better understanding of sweat allergy and therapeutic innovations.
Topics: Antigens, Fungal; Histamine Release; Humans; Hypersensitivity; Malassezia; Sweat
PubMed: 30075993
DOI: 10.1016/j.alit.2018.07.002 -
Canadian Medical Association Journal May 1973Protamine is used for titration of heparin in vitro for diagnosis of hemorrhagic states and for neutralization of heparin in vivo to terminate heparinization. The... (Review)
Review
Protamine is used for titration of heparin in vitro for diagnosis of hemorrhagic states and for neutralization of heparin in vivo to terminate heparinization. The protamine equivalent varies with the heparin preparation, conditions of testing and, in vivo, with the amount of heparin present in the circulation. The latter depends on time after administration and the hemodynamic and metabolic state of the patient. Protamine, when injected rapidly, will release histamine and agglutinate platelets. Bleeding (spontaneous hemorrhage) demonstrates a multiple breakdown of hemostatic mechanisms due to surgical stress, drugs, exposure of the blood to foreign surfaces, etc. Simple rules for the amount of protamine required for an individual patient based on clinical judgement will be satisfactory in most cases. When hemostasis is not achieved, it must be appreciated that heparin and protamine are only part of a complex deteriorating situation.
Topics: Hemorrhage; Hemostasis; Heparin; Heparin Antagonists; Histamine Release; Humans; Hypotension; In Vitro Techniques; Neutralization Tests; Protamines; Thrombocytopenia
PubMed: 4122234
DOI: No ID Found -
British Journal of Pharmacology Sep 2013The term 'neurogenic inflammation' has been adopted to describe the local release of inflammatory mediators, such as substance P and calcitonin gene-related peptide,... (Review)
Review
The term 'neurogenic inflammation' has been adopted to describe the local release of inflammatory mediators, such as substance P and calcitonin gene-related peptide, from neurons. Once released, these neuropeptides induce the release of histamine from adjacent mast cells. In turn, histamine evokes the release of substance P and calcitonin gene-related peptide; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established. The aim of this review is to summarize the most recent findings on the role of histamine in neurogenic inflammation, with particular regard to nociceptive pain, as well as neurogenic inflammation in the skin, airways and bladder.
Topics: Animals; Calcitonin Gene-Related Peptide; Histamine; Histamine Release; Humans; Mast Cells; Neurogenic Inflammation; Neurons; Nociceptive Pain; Substance P
PubMed: 23734637
DOI: 10.1111/bph.12266 -
Frontiers in Immunology 2022Chronic inducible urticaria (CIndU) constitutes a group of nine different CIndUs in which pruritic wheals and/or angioedema occur after exposure to specific and definite...
BACKGROUND
Chronic inducible urticaria (CIndU) constitutes a group of nine different CIndUs in which pruritic wheals and/or angioedema occur after exposure to specific and definite triggers. Histamine released from activated and degranulating skin mast cells is held to play a key role in the pathogenesis of CIndU, but evidence to support this has, as of yet, not been reviewed systematically or in detail. We aim to characterize the role and relevance of histamine in CIndU.
METHODS
We systematically searched 3 electronic databases (PubMed, Scopus, and Embase) for studies that reported increased serum or skin histamine concentration (direct evidence) or or histamine release (indirect evidence) following trigger exposure.
RESULTS
An initial total of 3,882 articles was narrowed down to 107 relevant studies of which 52 were in cold urticaria, 19 in cholinergic urticaria, 14 in heat urticaria, 10 in contact urticaria, 7 each in solar urticaria and vibratory angioedema, 4 each in symptomatic dermographism and aquagenic urticaria, and 3 in delayed pressure urticaria. The results of our review support that histamine has a key pathogenic role in the pathogenesis of all CIndUs, but it is not the sole mediator as evidenced by the often poor relationship between the level of histamine and severity of symptoms and the variable clinical efficacy of H-antihistamines.
CONCLUSIONS
Histamine released from skin mast cells is a key driver of the development of signs and symptoms and a promising therapeutic target in CIndU.
Topics: Angioedema; Chronic Urticaria; Histamine; Histamine Release; Humans; Urticaria
PubMed: 35967442
DOI: 10.3389/fimmu.2022.901851 -
Anaesthesia Jul 1993
Topics: Adult; Aged; Female; Histamine Release; Humans; Neuromuscular Blocking Agents
PubMed: 7688493
DOI: 10.1111/j.1365-2044.1993.tb07114.x -
Theoretical Biology & Medical Modelling Dec 2017Histamine (HA), a small molecule that is synthesized from the amino acid histidine, plays an important role in the immune system where it is associated with allergies,...
BACKGROUND
Histamine (HA), a small molecule that is synthesized from the amino acid histidine, plays an important role in the immune system where it is associated with allergies, inflammation, and T-cell regulation. In the brain, histamine is stored in mast cells and other non-neuronal cells and also acts as a neurotransmitter. The histamine neuron cell bodies are in the tuberomammillary (TM) nucleus of the hypothalamus and these neurons send projections throughout the central nervous system (CNS), in particular to the cerebral cortex, amygdala, basal ganglia, hippocampus, thalamus, retina, and spinal cord. HA neurons make few synapses, but release HA from the cell bodies and from varicosities when the neurons fire. Thus the HA neural system seems to modulate and control the HA concentration in projection regions. It is known that high HA levels in the extracellular space inhibit serotonin release, so HA may play a role in the etiology of depression.
RESULTS
We compare model predictions to classical physiological experiments on HA half-life, the concentration of brain HA after histidine loading, and brain HA after histidine is dramatically increased or decreased in the diet. The model predictions are also consistent with in vivo experiments in which extracellular HA is measured, using Fast Scan Cyclic Voltammetry, in the premammillary nucleus (PM) after a 2 s antidromic stimulation of the TM, both without and in the presence of the H autoreceptor antagonist thioperamide. We show that the model predicts well the temporal behavior of HA in the extracellular space over 30 s in both experiments.
CONCLUSIONS
Our ability to measure in vivo histamine dynamics in the extracellular space after stimulation presents a real opportunity to understand brain function and control. The observed extracellular dynamics depends on synthesis, storage, neuronal firing, release, reuptake, glial cells, and control by autoreceptors, as well as the behavioral state of the animal (for example, depression) or the presence of neuroinflammation. In this complicated situation, the mathematical model will be useful for interpreting data and conducting in silico experiments to understand causal mechanisms. And, better understanding can suggest new therapeutic drug targets.
Topics: Brain; Extracellular Space; Histamine; Histamine H3 Antagonists; Histamine Release; Humans; Models, Theoretical; Receptors, Histamine H3
PubMed: 29228949
DOI: 10.1186/s12976-017-0070-9 -
Veterinary Medicine and Science Jan 2021Canine mastocytomas (MCTs) are characterized by rapid proliferation of neoplastic mast cells (MCs) and clinical signs caused by MC-derived mediators. In dogs suffering...
Canine mastocytomas (MCTs) are characterized by rapid proliferation of neoplastic mast cells (MCs) and clinical signs caused by MC-derived mediators. In dogs suffering from MCT, histamine receptor 1 (HR1) antagonists are frequently used to control mediator-related clinical symptoms. Previous studies have shown that the HR1 antagonists loratadine and terfenadine exert some growth-inhibitory effects on neoplastic MCs. We examined whether other HR1 antagonists used in clinical practice (desloratadine, rupatadine, cyproheptadine, dimetindene, diphenhydramine) affect proliferation and survival of neoplastic MCs. Furthermore, we analysed whether these HR1 antagonists counteract IgE-dependent histamine release from a MC line harbouring a functional IgE-receptor. HR1 antagonists were applied on two canine MC lines, C2 and NI-1, and on primary MCs obtained from three MCT samples. The HR1 antagonists desloratadine, rupatadine and cyproheptadine were found to be more potent in decreasing proliferation of C2 and NI-1 cells when compared with dimetindene and diphenhydramine. Similar effects were seen in primary neoplastic MCs, except for diphenhydramine, which exerted more potent growth-inhibitory effects than the other HR1 antagonists. Drug-induced growth-inhibition in C2 and NI-1 cells was accompanied by apoptosis. Loratadine, desloratadine and rupatadine also suppressed IgE-dependent histamine release in NI-1 cells. However, drug concentrations required to elicit substantial effects on growth or histamine release were relatively high (>10 µM). Therefore, it remains unknown whether these drugs or similar, more potent, HR1-targeting drugs can suppress growth or activation of canine neoplastic MCs in vivo.
Topics: Animals; Cell Proliferation; Dogs; Histamine Antagonists; Histamine Release; Mast Cells
PubMed: 32924324
DOI: 10.1002/vms3.336 -
Molecular Pain Jul 2008Itch is one of the major complications of skin diseases. Although there are various substances that induce itch or pruritus, it is evident that histamine is the best... (Review)
Review
Itch is one of the major complications of skin diseases. Although there are various substances that induce itch or pruritus, it is evident that histamine is the best known endogenous agent that evokes itch. Even though histamine-induced itch has been studied for some time, the underlying mechanism of itch is just beginning to emerge. Although various downstream signaling pathways of histamine receptors have been revealed, more studies are required to determine the cause of histamine-induced itch. It appears that itch and pain involve different neuronal pathways. Pain generally inhibits itch, which indicates an inter-communication between the two. Complex interactions between itch and pain may be expected based on reports on disease states and opioids. In this review, we discuss the molecular mechanism and the pharmacological aspects of histamine-induced itch. Especially, the underlying mechanism of TRPV1 (an anti-pruritus target) has been determined to some extent.
Topics: Animals; Histamine Release; Humans; Pain; Pruritus
PubMed: 18667087
DOI: 10.1186/1744-8069-4-29 -
Journal of Applied Physiology... Feb 2022Aerobic exercise induces mast cell degranulation and increases histamine formation by histidine decarboxylase, resulting in an ∼150% increase in intramuscular...
Aerobic exercise induces mast cell degranulation and increases histamine formation by histidine decarboxylase, resulting in an ∼150% increase in intramuscular histamine. The purpose of this study was to determine if the increase in skeletal muscle temperature associated with exercise is sufficient to explain this histamine response. Specifically, we hypothesized that local passive heating that mimics the magnitude and time course of changes in skeletal muscle temperature observed during exercise would result in increased intramuscular histamine concentrations comparable to exercising values. Seven subjects participated in the main study in which pulsed short-wave diathermy was used to passively raise the temperature of the vastus lateralis over 60 min. Heating increased intramuscular temperature from 32.6°C [95% confidence interval (CI) 32.0°C to 33.2°C] to 38.9°C (38.7°C to 39.2°C) ( < 0.05) and increased intramuscular histamine concentration from 2.14 ng/mL (1.92 to 2.36 ng/mL) to 2.97 ng/mL (2.57 to 3.36 ng/mL) ( < 0.05), an increase of 41%. In a follow-up in vitro experiment using human-derived cultured mast cells, heating to comparable temperatures did not activate mast cell degranulation. Therefore, it appears that exercise-associated changes in skeletal muscle temperature are sufficient to generate elevations in intramuscular histamine concentration. However, this thermal effect is most likely due to changes in de novo histamine formation via histidine decarboxylase and not due to degranulation of mast cells. In conclusion, physiologically relevant increases in skeletal muscle temperature explain part, but not all, of the histamine response to aerobic exercise. This thermal effect may be important in generating positive adaptations to exercise training. The "exercise signal" that triggers histamine release within active skeletal muscle during aerobic exercise is unknown. By mimicking the magnitude and time course of increasing skeletal muscle temperature observed during aerobic exercise, we demonstrate that part of the exercise-induced rise in histamine is explained by a thermal effect, with in vitro experiments suggesting this is most likely via de novo histamine formation. This thermal effect may be important in generating positive adaptations to exercise training.
Topics: Heating; Histamine; Histamine Release; Humans; Hyperthermia, Induced; Muscle, Skeletal
PubMed: 34941436
DOI: 10.1152/japplphysiol.00740.2021 -
The Yale Journal of Biology and Medicine 1992The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A... (Review)
Review
The regulation of histamine release from oxyntic mucosa is complex because of two potential sources of histamine: mast cells and enterochromaffin-like (ECL) cells. A gastrin-responsive histamine pool was identified in the rat oxyntic mucosa two decades ago, but these ECL cells from the rat have not yet been isolated or characterized in vitro. In vivo studies in canine and human mucosa have been more difficult because of the high content of histamine in mast cells. Using enzyme-dispersed canine oxyntic mucosal cells, we have studied regulation of histamine release from a mast cell-depleted fraction prepared by sequential elutriation and density gradient. Histamine-like immunoreactivity was demonstrated, using peroxidase-anti-peroxidase immunohistochemistry. After short-term culture, histamine was released in response to gastrin, cholecystokinin, carbachol, and forskolin. Somatostatin potently and effectively inhibited the response to gastrin. The cultures used for these studies also contained somatostatin cells, and, furthermore, the response to gastrin was enhanced by incubation with monoclonal antibodies to somatostatin. The latter findings suggested that somatostatin was acting in these cultures by a paracrine route. This pattern contrasts with that obtained in previous studies of canine oxyntic mucosal mast cells.
Topics: Animals; Dogs; Gastric Mucosa; Histamine Release; Humans; Parietal Cells, Gastric; Rats
PubMed: 1285199
DOI: No ID Found