Systematic comparisons of various markers for mast cell activation in RBL-2H3 cells

Rujitharanawong, Chuda; Yoodee, Sunisa; Sueksakit, Kanyarat; Peerapen, Paleerath; Tuchinda, Papapit; Kulthanan, Kanokvalai; Thongboonkerd, Visith

doi:10.1007/s00441-022-03687-w

Cited by 7 publications

(2 citation statements)

References 89 publications

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“…This leads to the releases of vesicle-stored allergic mediators, such as histamine, leukotriene D4, chemokines, cytokines, and neutral proteases ( Ando and Kitaura, 2021 ). The most popular method for assessing mast cell degranulation is to measure β-hexosaminidase activity in RBL-2H3 mast cells after exposure to human serum albumin (HSA, antigen) ( Rujitharanawong et al ., 2022 ). Elafibranor inhibited HSA-induced release of β-hexosaminidase in a concentration-dependent manner ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Elafibranor PPARα/δ Dual Agonist Ameliorates Ovalbumin-Induced Allergic Asthma

Lee,

2024

Biomol Ther (Seoul)

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Asthma is characterized by chronic inflammation and respiratory tract remodeling. Peroxisome proliferator-activated receptors (PPARs) play important roles in the pathogenesis and regulation of chronic inflammatory processes in asthma. The role of PPARγ has been studied using synthetic PPARγ agonists in patients with asthma. However, involvement of PPARα/δ has not been studied in asthma. In the present study, we investigated if elafibranor, a PPARα/δ dual agonist, can modulate ovalbumin (OVA)-induced allergic asthma, which is a potential drug candidate for non-alcoholic fatty liver in obese patients. Elafibranor suppresses antigen-induced degranulation in RBL-2H3 mast cells without inducing cytotoxicity in vitro . In mice with OVA-induced allergic asthma, the administration of elafibranor suppressed OVA-induced airway hyper-responsiveness at a dose of 10 mg/kg. Elafibranor also suppressed the OVA-induced increase in immune cells and pro-inflammatory cytokine production in the bronchoalveolar lavage fluid (BALF). Histological studies suggested that elafibranor suppressed OVA-induced lung inflammation and mucin hyper-production in the bronchial airways. In addition, elafibranor suppressed OVA-induced increases in serum immunoglobulin E and IL-13 levels in BALF. Conversely, the present study suggests that elafibranor has the potential for use in patients with allergic asthma.

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Section: Resultsmentioning

confidence: 99%

Elafibranor PPARα/δ Dual Agonist Ameliorates Ovalbumin-Induced Allergic Asthma

Lee,

2024

Biomol Ther (Seoul)

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“…Indeed, as our intent was to investigate the occurrence and spatial distribution of mast cells in nasal mucosa, we excluded traditional histological stains, such as Toluidine blue and Giemsa, which allow to identify the intact MCs but not those in degranulation. Thus, we evaluated by immunohistochemistry the expression of two markers of MCs 12 : CD-117 (c-kit receptor), which is strongly expressed on the mast cell membrane and is not affected by the state of degranulation, to determine the presence of MCs and obtain the MC count 13 ; Tryptase, which is considered as the marker of choice for the study of mast cell activation, to evaluate the degree of degranulation and, in a certain extent, mast cells activity 14 .…”

Section: Methodsmentioning

confidence: 99%

Eosinophil-mast cell pattern of intraepithelial infiltration as a marker of severity in CRSwNP

Gelardi,

Giancaspro,

Duda

et al. 2023

Sci Rep

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Chronic rhinosinusitis with nasal polyps (CRSwNP) is defined as a Type 2 eosinophilic disease, while CRSsNP is considered a Type 1 neutrophilic disease. Since neutrophils are also activated in eosinophilic CRSwNP, the eosinophil–neutrophil dualism has been revaluated. Among the inflammatory cells infiltrating sinus-nasal tissues, the role of mast cells (MCs) is not already recognized, although Clinical-Cytological Grading, which defines the severity of CRSwNP, attributes to mixed eosinophil-MC forms of CRSwNP a greater risk of recurrence. We aimed to examine nasal polyps from both a cytological and histopathological point of view, to evaluate the presence and localization of MCs. Cytological and histological examination of 39 samples of nasal polyps were performed. Immunohistochemistry was used to evaluate the presence of Tryptase + CD117 + MCs, which were counted both in the epithelial layer and in the lamina propria. A statistically significant correlation was found between intraepithelial MCs and CRSwNP severity (p < 0.001) and between the total eosinophil count and the total mast cell count (p < 0.001). Cytological examination and immunohistochemistry were comparable in detecting the presence of intraepithelial MCs (p = 0.002). The histological cut-off of 6 intraepithelial MCs was identified to detect severe CRSwNP (p < 0.001). MCs have been shown to be located in the lamina propria of almost all eosinophilic nasal polyps without significantly affecting their severity. Intraepithelial MCs are associated with greater severity of CRSwNP. Histopathological criteria of the eosinophil-MC form of CRSwNP in addition to the eosinophilic one, should be defined to guarantee patients effective and tailored treatments.

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Surface charge, but not size, of liposomes is involved in the suppression of rat basophilic leukemia (RBL‐2H3) cell degranulation mediated by Akt phosphorylation

Inoh,

Ito,

Yokawa

et al. 2024

Cell Biology International

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Cationic liposomes composed of cholesteryl‐3β‐carboxyamidoethylene‐N‐hydroxyethylamine (OH‐chol) and 1,2‐dioleoyl‐sn‐glycero‐3‐phosphatidylethanolamine (DOPE) inhibit mast cell degranulation mediated via crosslinking of high‐affinity IgE receptors (FcεRI). Although the inhibitory efficiency of mast cell degranulation is altered by modifying the ratio of OH‐chol and DOPE in cationic liposomes, the manner in which physicochemical properties, such as surface charge and size, influence suppression is not clear. We observed that positive surface charge, but not the size, of liposomes plays a role in suppressing rat basophilic leukemia (RBL‐2H3) cell activation. Pretreatment with middle‐ratio OH‐chol liposomes (zeta potential, 62.2 ± 0.5 mV; diameter, 325.4 ± 7.3 nm) exhibited a larger suppression of RBL‐2H3 cell degranulation evoked by FcεRI crosslinking compared with that by low‐ratio OH‐chol liposomes (zeta potential, 48.6 ± 1.9 mV; diameter, 344.4 ± 25.0 nm), although both liposomes were similarly attached to RBL‐2H3 cells. Preparation of middle‐ratio OH‐chol liposomes, classified roughly by size using an extrusion method, revealed that the liposomal size did not affect the inhibitory efficiency of RBL‐2H3 cell activation. Mechanistically, we found that middle‐ratio OH‐chol liposomes increased the inhibition of antigen‐induced Akt phosphorylation compared to low‐ratio OH‐chol liposomes. We measured the phosphorylation of linker for activation of T cells (LAT) and paxillin, which are important proteins in FcεRI‐ and focal adhesions (FAs)‐mediated signaling, respectively. Middle ratio OH‐chol liposomes significantly suppressed antigen‐induced paxillin phosphorylation, but did not affect LAT phosphorylation, suggesting that middle‐ratio OH‐chol liposomes attached to RBL‐2H3 cells suppress the degranulation by impairing FA‐mediated Akt phosphorylation evoked by FcεRI crosslinking.

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Systematic comparisons of various markers for mast cell activation in RBL-2H3 cells

Cited by 7 publications

References 89 publications

Elafibranor PPARα/δ Dual Agonist Ameliorates Ovalbumin-Induced Allergic Asthma

Elafibranor PPARα/δ Dual Agonist Ameliorates Ovalbumin-Induced Allergic Asthma

Eosinophil-mast cell pattern of intraepithelial infiltration as a marker of severity in CRSwNP

Surface charge, but not size, of liposomes is involved in the suppression of rat basophilic leukemia (RBL‐2H3) cell degranulation mediated by Akt phosphorylation

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