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Mast cell activation syndrome:An up-to-date review of literature

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World Journal of Clinical Pediatrics 2024年第2期13卷 104-113页

作者： ÖnerÖzdemir Gökçe Kasımoğlu Ayşegül Bak Hüseyin Sütlüoğlu Süreyya Savaşan Department of Pediatric Allergy and Immunology Sakarya UniversitySakaryaAdapazarı54100Türkiye Department of Pediatrics Sakarya UniversitySakaryaAdapazarı54100Türkiye Department of Pediatrics Kocaeli City HospitalKocaeli 50123Türkiye Department of Pediatrics Children’s Hospital of MichiganHematology/OncologyCentral Michigan University College of MedicineMount PleasantMI 48859United States Barbara Ann Karmanos Cancer Institute Wayne State UniversityDetroitMI 12345United States

Mast cells are a subtype of white blood cells and are involved in the immune system.These cells contain many chemical substances called mediators,which are involved in the allergic response.The fact that mast cells play a role in many events that require urgent intervention,especially anaphylaxis,has led to a more detailed study of these cells.The diseases also caused by dysfunctions of mast cells have been examined in many circumstances.For instance,mast cell activation syndrome is known as an augmented number of cells due to decreased cell death,resulting in clinical symptoms affecting many systems.The main common symptoms include flushing,hypotension,urticaria,angioedema,headache,vomiting and diarrhea.Although the underlying mechanism is not yet clearly known,we aim to review the literature in a broad perspective and bring together the existing knowledge in the light of the literature due to the diversity of its involvement in the body and the fact that it is a little known syndrome.

关键词： Mast cell Mast cell activation syndrome Tryptase histamine

histamine Excites Rat GABAergic Ventral Pallidum Neurons via Co-activation of H1 and H2 Receptors

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Neuroscience Bulletin 2018年第6期34卷 1029-1036页

作者： Miao-Jin Ji Xiao-Yang Zhang Xiao-Chun Peng Yang-Xun Zhang Zi Chen Lei Yu Jian-Jun Wang Jing-Ning Zhu State Key Laboratory of Pharmaceutical Biotechnology and Department of Physiology School of Life Sciences Nanjing University

The ventral pallidum(VP) is a crucial component of the limbic loop of the basal ganglia and participates in the regulation of reward, motivation, and emotion.Although the VP receives afferent inputs from the central histaminergic system, little is known about the effect of histamine on the VP and the underlying receptor mechanism. Here, we showed that histamine, a hypothalamicderived neuromodulator, directly depolarized and excited the GABAergic VP neurons which comprise a major cell type in the VP and are responsible for encoding cues of incentive salience and reward hedonics. Both postsynaptic histamine H1 and H2 receptors were found to be expressed in the GABAergic VP neurons and co-mediate the excitatory effect of histamine. These results suggested that the central histaminergic system may actively participate in VP-mediated motivational and emotional behaviors via direct modulation of the GABAergic VP neurons. Our findings also have implications for the role of histamine and the central histaminergic system in psychiatric disorders.

关键词： Ventral pallidum histamine H1 receptor H2 receptor Motivation Emotion

Facilitating effect of histamine on spatial memory deficits induced by dizocilpine as evaluated by 8-arm radial maze in SD rats

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Acta Pharmacologica Sinica 2003年第12期24卷 96-102页

作者： HUANG Yu-Wen, CHEN Zhong~2, HU Wei-Wei, ZHANG Li-San, WU Wei, YING Li-Yang, WEI Er-Qing Department of Neurobiology and Pharmacology, School of Medicine, Zhejiang University, Hangzhou 310031, China Department of Neurobiology and Pharmacology School of Medicine Zhejiang University Hangzhou 310031

AIM: To investigate whether or not histamine is involved in spatial memory deficits induced by dizocilpine (MK-801) as evaluated by 8-arm radial maze of rats. METHODS: 8-Arm (4-arm baited) radial maze was used to measure spatial memory in rats. RESULTS: Bilaterally intrahippocampal (ih) injection of MK-801 (0.3 μg/site) impaired working memory and reference memory in rats. Both histamine (50, 100 ng/site, ih) and intraperitoneal (ip) injection of histidine (100, 200 mg/kg) markedly improved the spatial memory deficits induced by MK-801. On the other hand, the ameliorating effect of histidine (100 mg/kg, ip) was completely antagonized by α-fluoromethylhistidine (α-FMH, 5 μg/site, ih), a potent and selective histidine decarboxylase (HDC) inhibitor, and H1-antagonist pyrilamine (1 μg/site, ih), but not by H2-antagonist cimetidine, even at a high dose (2.5 μg/site, ih). CONCLUSION: The hippocampal histamine plays an important role in the ameliorating effect on MK-801-induced spatial memory deficits,

关键词： histamine maze learning dizocilpine memory disorders

Isoquercitrin suppresses the expression of histamine and pro-inflammatory cytokines by inhibiting the activation of MAP Kinases and NF-κB in human KU812 cells

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Chinese Journal of Natural Medicines 2016年第6期14卷 407-412页

作者： LI Li ZHANG Xiao-Hui LIU Guang-Rong LIU Chang DONG Yin-Mao Beijing Key Laboratory of Plant Resources Research and Development Beijing Technology and Business UniversityBeijing100048China Infinitus(China)Company Ltd. Guangzhou 510665China

Mast cells and basophils are multifunctional effector cells that contain abundant secretory granules in their cytoplasm. Both cell types are involved in a variety of inflammatory and immune events, producing an array of inflammatory mediators, such as cytokines. The aim of the study was to examine whether isoquercitrin modulates allergic and inflammatory reactions in the human basophilic KU812 cells and to elucidate its influence on the phosphorylation of mitogen-activated protein kinase(MAPK) and nuclear factor(NF)-κB activation. The KU812 cells were stimulated with phorbol-12-myristate 13-acetate plus the calcium ionophore A23187(PMACI). The inhibitory effects of isoquercitrin on the productions of histamine and pro-inflammatory cytokines in the stimulated KU812 cells were measured using cytokine-specific enzyme-linked immunosorbent(ELISA) assays. Western blotting analysis was used to assess the effects of isoquercitrin on the MAPKs and NF-κB protein levels. Our results indicated that the isoquercitrin treatment of PMACI-stimulated KU812 cells significantly reduced the production of histamine and the pro-inflammatory cytokines, such as interleukin(IL)-6, IL-8, IL-1β, and tumor necrosis factor(TNF)-α. The treated cells exhibited decreased phosphorylation of extracellular signal-regulated kinase(ERK), revealing the role of ERK MAPK in isoquercitrin-mediated allergy inhibition. Furthermore, isoquercitrin suppressed the PMACI-mediated activation of NF-κB in the human basophil cells. In conclusion, the results from the present study provide insights into the potential therapeutic use of isoquercitrin for the treatment of inflammatory and allergic reactions.

关键词： Isoquercitrin,KU812 cells histamine Cytokines Mitogen-activated protein kinase Nuclear factor-κB

Effects of histamine on spontaneous neuropathic pain induced by peripheral axotomy

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Neuroscience Bulletin 2013年第3期29卷 261-269页

作者： Jie Yu Guo-Dong Lou Jia-Xing Yue Ying-Ying Tang Wei-Wei Hou Wen-Ting Shou Hiroshi Ohtsu Shi-Hong Zhang Zhong Chen Department of Pharmacology School of Basic Medical Sciences College of Pharmaceutical Sciences Zhejiang University School of Pharmaceutical Sciences Wenzhou Medical College Department of Engineering School of Medicine Tohoku University

The present study was designed to investigate the effects of histamine on spontaneous neuropathic pain （NP） induced by peripheral axotomy. Rats and mice were subjected to complete transection of the left sciatic and saphenous nerves to induce spontaneous NP （the neuroma model）. Rats were then treated with drugs once daily for 30 days （histidine and Ioratadine, i.p.） or 21 days （histamine, i.c.v.）. Autotomy behavior was scored daily until day 50 postoperation （PO）. On days 14 to 21 PO, some rats in the control group were subjected to singlefiber recording. Autotomy behavior was also monitored daily in histidine decarboxylase （the key enzyme for histamine synthesis） knockout （HDC/） and wildtype mice for 42 days. We found that both histidine （500 mg/kg）（a precursor of histamine that increases histamine levels in the tissues） and histamine （50 pg/5 pL） significantly suppressed autotomy behavior in rats. HDC mice lacking endogenous histamine showed higher levels of autotomy than the wildtype. In addition, the analgesic effect of histidine was not antagonized by Ioratadine （a peripherallyacting H1 receptor antago nist）, while Ioratadine alone significantly suppressed autotomy. Electrophysiological recording showed that ectopic spontaneous discharges from the neuromawere blocked by systemic diphenhydramine （an H receptor antagonist）. Our results suggest that hista mine plays an important role in spontaneous NP. It is likely that histamine in the central nervous system is analgesic, while in the periphery, via H receptors, it is algesic. This study justifies the avoidance of a histaminerich diet and the use of peripherallyacting H receptor antagonists as well as agents that improve histamine action in the central nervous system in pa tients with spontaneous NP.

关键词： histamine Ioratadine H1 receptor neuropathic pain

Stimulation by nizatidine,a histamine H_2-receptor antagonist,of duodenal HCO_3^-secretion in rats:relation to anti-cholinesterase activity

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World Journal of Gastroenterology 2000年第5期6卷 651-658页

作者： Koji Takeuchi Shoji Kawauchi Hideo Araki Shigeru Ueki Osamu Furukawa Department of Pharmacology and Experimental Therapeutics Kyoto Pharmaceutical UniversityMisasagiYamashinaKyoto 607-8414Japan CURE Bldg.114Suite 217 West LA VAMC 11301 Wilshire Blvd.Los AngelesCA 90073

AIM To examine whether nizatidine stimulatesduodenal HCO3- secretion in rats by inhibitingAChE activity.METHODS Under pentobarbital anesthesia,aproximal duodenal loop was perfused withsaline,and the HCO3 secretion was measuredat pH 7.0 using a pH-stat method and by adding10mM HCI.Nizatidine,neostigmine,carbacholor famotidine was administered i.***.as a singleinjection.RESULTS Intravenous administration ofnizatidine（3-30 mg/kg）dose-dependentlyincreased duodenal HCO3- secretion,and theeffect at 10mg/kg was equivalent to thatobtained by carbachol at 0.01 mg/kg.Thisnizatidine action was observed at the same doserange that inhibited acid secretion and enhancedgastric motility,mimicked by i.***.injection ofneostigmine（0.03 mg/kg）,and significantlyattenuated by bilateral vagotomy and prior s.***.administration of atropine but not byindomethacin,a cyclooxygenase inhibitor,orNG-nitro-L-arginine methyl ester,a NO synthaseinhibitor.The HCO3- secretory response toacetylcholine（0.001 mg/kg）was significantlypotentiated by the concurrent administration ofnizatidine（3mg/kg,i.v.）.The IC50of nizatidine for AChE of rat erythrocytes was1.4×10-6M,about 12 times higher than that ofneostigmine.Neither famotidine(>10-3M,30mg/kg,i.v.)nor cisapride(> 10-3M,3mg/kg,i.v.)had any influence on AChEactivity or duodenal HCO3- secretion.Duodenaldamage induced by acid perfusion（100 mM HCIfor 4 h）in the presence of indomethacin wassignificantly prevented by nizatidine andneostigmine,at the doses that increased theHCO3- secretion.CONCLUSION Nizatidine stimulates duodenalHCO3- secretion,in both vagal-dependent andatropine-sensitive manners,and the action isassociated with the anti-AChE activity of thisagent.

关键词： nizatidine histamine H2 receptor blockaders duodenal HCO3-secretion cholinesterase inhibitors rats

Passive sensitization increases histamine-stimulated calcium signaling and NF-κB transcription activity in bronchial epithelial cells

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Acta Pharmacologica Sinica 2006年第6期27卷 708-714页

作者： Si JIN~(2,5)Dan TIAN~3 Jian-guo CHEN~4 Li-ping ZHU~2 Sheng-yuan LIU~2 Di-xun WANG~2 2 Department of Pathophysiology,Tongji Medical College,Huazhong University of Science and Technology Key Laboratory of Pulmonary Disease of Ministry of Health of China,Wuhan 430030,China 3 Department of Pathology,Tongji Medical College.Huazhong University of Science and Technology.Wuhan 430030,China 4 Department of Pharmacology,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China Department of Pathophysiology Tongji Medical College Huazhong University of Science and Technology Key Laboratory of Pulmonary Disease of Ministry of Health of China Wuhan China Department of Pathology Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of Pharmacology Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To find out if the two aspects of asthma（chronic airway inflammation andbronchial hyperresponsiveness）are related to hypersensitivity of calcium signal-ing in bronchial epithelial cells.Methods:Porcine bronchial epithelial cells（PBEC）were divided into sensitized（S）and nonsesitized（N）groups.In group S,the cellswere preincubated with serum from ovalbumin sensitized guinea pigs.In group N,the cells were preincubated with serum from nonsensitized guinea pigs.Singlecell calcium imaging and ELISA-based NF-κ3 activity were used to evaluate thehistamine-stimulated intracellular free calcium level and NF-κB activity,respectively.Results:First,0.1μmol/L histamine could induce [Ca2+]ioscillationsin PBEC of group S,but not in group N.Second,1/Jmol/L histamine could induce[Ca2+]ioscillations of PBEC in both group S and group N.The [Ca2+]ioscillationfrequency of PBEC was significantly higher in group S than in group N,thoughthe[Ca2+]ioscillation amplitude showed no difference between the two groups.Finally,when 10 μmol/L histamine was used to stimulate PBEC a transient initialincrease followed by a sustained elevation（FSE）of [Ca2+]iwas observed in PBECin both groups.The amplitude of the FSE of [Ca2+]iin PBEC was significantlyhigher in group S than in group N.The subsequent NF-κB activity was in accor-dance to the calcium oscillation frequency evoked by histamine,but not to theamplitude.Conclusion:It was suggested that the increased sensitivity of calciumsignaling in bronchial epithelial cells might contribute to the exorbitant inflamma-tion or increased susceptibility in asthmatic airway epithelial cells.

关键词： asthma histamine calcium signaling bronchi epithelial cell nuclear factor of kappaB

Orexin A promotes histamine,but not norepinephrine or serotonin,release in frontal cortex of mice

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Acta Pharmacologica Sinica 2005年第2期26卷 155-159页

作者： Zong-yuan HONG~(2.3),Zhi-li HUANG~(3,4,5),Wei-min QU~3,Naomi EGUCHI~3~2School of Life Science,University of Science and Technology of China,Hefei 230027,China ~3Department of Molecular Behavioral Biology,Osaka Bioscience Institute,Furuedai,Suita,Osaka 565-0874,Japan ~4Department of Pharmacology,Shanghai Medical College of Fudan University,Shanghai 200032,China School of Life Science University of Science and Technology of China Hefei China Department of Molecular Behavioral Biology Osaka Bioscience Institute Furuedai Suita Japan Department of Pharmacology Shanghai Medical College of Fudan University Shanghai China

Aim:To investigate the effects of orexin A on release of histamine,norepinephrine,and serotonin in the frontal cortex of mice.Methods:Samples for measuringhistamine,norepinephrine,and serotonin contents were collected by in vivomicrodialysis of the frontal cortex of anesthetized mice.The histamine,noradrenaline,and serotonin content in dialysates were measured by HPLCtechniques.Results:Intracrebroventricular injection of orexin A at doses of 12.5,50,and 200 pmol per mouse promoted histamine release from the frontal cortex ina dose-dependent manner.At the highest dose given,200 pmol,orexin A signifi-cantly induced histamine release,with the maximal magnitude being 230% overthe mean basal release.The enhanced histamine release was sustained for 140min,and then gradually returned to the basal level.However,no change in nore-pinephrine or serotonin release was observed under application of the same doseof orexin A.Conclusion:These results suggest that the arousal effect of orexin Ais mainly mediated by histamine,not by norepinephrine or serotonin.

关键词： orexin A histamine noradrenaline serotonin microdialysis frontal cortex

An Experimental Study on the Disorders of Hepatic Hemodynamics and Changes of Plasma histamine in Dogs with Fulminant Hepatic Failure

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1998年第1期18卷 33-36页

作者：张柳清赵秋 Department of Pediatrics Tongji Hospital Tongji Medical University Wuhan Department of Gastroenterology Wuhan General Hospital of PLA Wuhan

The model of fulminant hepatic failure induced by acetaminophen was established in dogs to observe the changes of hepatic hemodynamics and plasma histamine levels in portal vein (PV), hepatic vein (HV), abdominal aorta (AA) and inferior vena cava (ICV). The results showed that the portal vein resistance (PVR) was elevated and portal venous blood flow (PVF) was decreasedl hepatic artery resistance (HAR) was decreased and the hepatic artery blood flow (HAF),portal venous pressure (PVP), wedged hepatic venous pressure (WHVP) and inferior vena cava pressure (ICVP) had no changes. The histamine of the PV, HV,ICV and AA were all elevated after formation of fulminant hepatie failure. And the increasing wave Of the HV was the highest. The increased histamine in HV may be mediated by H, receptor.causing the contraction of hepatic venulae, result ing liver sinusoid congestion, increasing PVR and decreasing PVF which exacerbate the liver cell damage. Moreover, the more selvere liver damage, the more histamine was released, and a vicious circle may ensue. Our results also suggest the possibility of using,H1 receptor antagonist to treat the disturbance of liver hemodynamfics in severe acute liver damage. The increased histamine in systematic circulation as a vasodilator may lower blood pressure and accelerate heart beats.The increase of plasma histamine may play an important role in the changes of hepatic and systemic hemodynamics in fulminant hepatic failure.

关键词： histamine fulminant hepatic failure acetaminophen