Histamine Release from Mast Cells and Basophils

Borriello, Francesco; Iannone, Raffaella; Marone, Gianni

doi:10.1007/164_2017_18

Cited by 78 publications

(69 citation statements)

References 135 publications

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“…These cells also express receptors for vascular endothelial growth factors (VEGFR1 and VEGFR2), and VEGFR co-receptors, neuropilin-1 and neuropilin-2 (NRP1 and NRP2), for anaphylatoxins (C5aR1/CD88, C5aR2, and C3aR), and the high-affinity urokinase plasminogen activator receptor (uPAR). Human mast cells also express co-receptors for T-cell activation [CD40 ligand (CD40L), tumor necrosis factor superfamily member 4 (OX40L), inducible costimulator ligand (ICOS-L), programmed death ligands (PD-L1 and PD-L2)] [Slightly modified with permission of Springer Nature from Borriello et al (15)].…”

Section: Introductionmentioning

confidence: 99%

Are Mast Cells MASTers in Cancer?

et al. 2017

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Prolonged low-grade inflammation or smoldering inflammation is a hallmark of cancer. Mast cells form a heterogeneous population of immune cells with differences in their ultra-structure, morphology, mediator content, and surface receptors. Mast cells are widely distributed throughout all tissues and are stromal components of the inflammatory microenvironment that modulates tumor initiation and development. Although canonically associated with allergic disorders, mast cells are a major source of pro-tumorigenic (e.g., angiogenic and lymphangiogenic factors) and antitumorigenic molecules (e.g., TNF-α and IL-9), depending on the milieu. In certain neoplasias (e.g., gastric, thyroid and Hodgkin’s lymphoma) mast cells play a pro-tumorigenic role, in others (e.g., breast cancer) a protective role, whereas in yet others they are apparently innocent bystanders. These seemingly conflicting results suggest that the role of mast cells and their mediators could be cancer specific. The microlocalization (e.g., peritumoral vs intratumoral) of mast cells is another important aspect in the initiation/progression of solid and hematologic tumors. Increasing evidence in certain experimental models indicates that targeting mast cells and/or their mediators represent a potential therapeutic target in cancer. Thus, mast cells deserve focused consideration also as therapeutic targets in different types of tumors. There are many unanswered questions that should be addressed before we understand whether mast cells are an ally, adversary, or innocent bystanders in human cancers.

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Section: Introductionmentioning

confidence: 99%

Are Mast Cells MASTers in Cancer?

et al. 2017

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“…Given that histamine is mainly released by the activated mast cells (Borriello et al, 2017), we firstly determined whether QKLI could directly promote mast cell degranulation. As shown in Figure 4A, 10 mg/ml of C48/80 evoked a markedly bhexosaminidase release in both human LAD2 cells and mouse peritoneal mast cells, while QKLI could not induce mast cell degranulation.…”

Section: Qkli Triggers Na-ihr By Activating Anaphylatoxin C3mentioning

confidence: 99%

Qing-Kai-Ling Injection Induces Immediate Hypersensitivity Reaction via the Activation of Anaphylatoxin C3

Gao

Zhang

et al. 2020

Front. Pharmacol.

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Background and Objective: Qing-Kai-Ling (QKL) is derived from a famous ancient Chinese patent medicine Angong Niuhuang pills (ANP) which has been used across Asia, especially in China, for the treatment of "febrile disease," such as stroke, encephalitis and meningitis for hundreds of years. As an extract of ANP without heavy metal, the clinical applicability of QKL is more intensive, of which its injection is commonly used in acute and serious diseases. This study aims to clarify the potential mechanisms of immediate hypersensitivity reaction (IHR) induced by QKL injection (QKLI). Methods: b-hexosaminidase release assay was performed on the human mast cell line LAD2 and mouse peritoneal mast cells. T helper 2 (Th2) immunity-amplified mice were prepared by aluminum adjuvant. Anaphylactic shock was detected by measuring rectal thermometry in propranolol-pretreated mice. For evaluating microvascular permeability, Evans Blue extravasation assay was used. Serum total IgE (tIgE) and the activated complement-derived anaphylatoxin C3 (C3a) levels were measured by ELISA. Results: QKLI was unable to elevate serum tIgE level in the Th2 immunity-amplified mice, but can increase vasopermeability and trigger anaphylaxis after the first injection. By screening seven fractions of QKLI, only the extract of Isatidis Radix (Isatis tinctoria L.) induced hindpaw Evans Blue extravasation, which was disappeared in Isatidis Radix-free QKLI. Mechanism study indicated that QKLI or Isatidis Radix-caused IHR could be blocked by the antagonists for histamine or C3a, rather than PAF or C5a. Consistently, QKLI and Isatidis Radix could also directly activate human serum complement-derived anaphylatoxin 3 (C3) in vitro with the half effective concentration values of 0.69% and 218.6 mg/ml, respectively. Conclusion: QKLI-IHR is complement activation-related pseudoallergy, rather than an IgE-mediated allergy. QKLI activates C3 and might consequently provoke mast cells to release histamine, which is a principal effector of its IHR. The pseudoallergic reaction induced by QKLI was attributed to the extract of Isatidis Radix. This study suggests a potential therapeutic strategy for the prophylaxis and treatment of QKLI-IHR.

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“…We also checked histamine release and ROS production induced by each particle. Histamine is one of the chemical mediators produced during an inflammatory response and is mainly secreted from basophils and mast cells [41]. Histamine release upon treatment with microparticles is shown in Fig.…”

Section: Histamine Release and Ros Production By Pe Microplastics Trementioning

confidence: 99%

Statistical Curvature Change Analysis of Random-Shape Polyethylene Microplastics and their Toxicity from a Physical Perspective

Choi

Hwang

Bang

et al. 2020

Preprint

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BackgroundMicroplastics,plastics thathave gradually and randomly decomposed into small fragmentsafter exposure to physical and biological external stress,are emerging as a significant environmental threat. They are normally categorized into the following three types: particles, fibers, and random-shape fragments brokendown from bulk plastics. Here, we have demonstrated the in vitro toxicity of microplastics of two different shapes. To minimize the chemical effect, polyethylene (PE),which has abasic chemical polymer structure,was used. PE microplastics withtwo different shapes were prepared,high-density PE (HDPE) microbeads and randomly ground low-density PE (LDPE) from bulk pellets.ResultsTo quantify the randomness of the microplastic shape, the edge patterns of the generated PE microplasticswere converted into numerical values and analyzed using a statistical method. A10-fold difference in curvature value was observed between PE particles and ground PE microfragments. We found that the higher concentration and rough structure were associated with the toxicity of plastics toward immune- or non-immune cells, pro-inflammatory cytokinerelease, and hemolysis, even though PE is buoyant onto medium. The smooth PE particles did not exhibit severe cytotoxicity at any of the tested concentrations, but induced immune and hemolysis responses at high concentrations. ConclusionWhen comparing the toxicity of two different shapes of PE microplastics, we confirmed by statistical analysis that random-shape plastics with sharp edges and higher curvature differences may adversely affect human cells.

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Histamine Release from Mast Cells and Basophils

Cited by 78 publications

References 135 publications

Are Mast Cells MASTers in Cancer?

Are Mast Cells MASTers in Cancer?

Qing-Kai-Ling Injection Induces Immediate Hypersensitivity Reaction via the Activation of Anaphylatoxin C3

Statistical Curvature Change Analysis of Random-Shape Polyethylene Microplastics and their Toxicity from a Physical Perspective

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