RBL-2H3 Mast Cells Research Articles

SGLT2 Inhibitors Empagliflozin and Canagliflozin Ameliorate Allergic Asthma Responses in Mice.

Inhibitors of sodium/glucose cotransporter 2 (SGLT2), such as empagliflozin and canagliflozin, have been widely used to block glucose reabsorption in the proximal tubules of kidneys in patients with diabetes. A meta-analysis suggested that SGLT2 inhibitors are associated with a decreased risk of asthma development. Therefore, we investigated whether SGLT2 inhibitors could suppress allergic asthma. Empagliflozin and canagliflozin suppressed the in vitro degranulation reaction induced by antigens in a concentration-dependent manner in RBL-2H3 mast cells. Empagliflozin and canagliflozin were administered to BALB/c mice sensitized to ovalbumin (OVA). The administration of empagliflozin or canagliflozin significantly suppressed OVA-induced airway hyper-responsiveness and increased the number of immune cells and pro-inflammatory cytokine mRNA expression levels in bronchoalveolar lavage fluid. The administration of empagliflozin and canagliflozin also suppressed OVA-induced histopathological changes in the lungs. Empagliflozin and canagliflozin also suppressed serum IgE levels. These results suggested that empagliflozin and canagliflozin may be applicable for the treatment of allergic asthma by suppressing immune responses.

Selonsertib, an ASK1 Inhibitor, Ameliorates Ovalbumin-Induced Allergic Asthma during Challenge and Sensitization Periods.

Apoptosis signal-regulating kinase 1 (ASK1) is an upstream signaling molecule in oxidative stress-induced responses. Because oxidative stress is involved in asthma pathogenesis, ASK1 gene deficiency was investigated in animal models of allergic asthma. However, there is no study to investigate whether ASK1 inhibitors could be applied for asthma to date. Selonsertib, a potent and selective ASK1 inhibitor, was applied to BALB/c mice of an ovalbumin (OVA)-induced allergic asthma model. Selonsertib suppressed antigen-induced degranulation of RBL-2H3 mast cells in a concentration-dependent manner. The administration of selonsertib both before OVA sensitization and OVA challenge significantly reduced airway hyperresponsiveness, and suppressed eosinophil numbers and inflammatory cytokine levels in the bronchoalveolar lavage fluid. Histopathologic examination elucidated less inflammatory responses and reduced mucin-producing cells around the peribronchial regions of the lungs. Selonsertib also suppressed the IgE levels in serum and the protein levels of IL-13 in the bronchoalveolar lavage fluid. These results suggest that selonsertib may ameliorate allergic asthma by suppressing immune responses and be applicable to allergic asthma.

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

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.

Aspalathin, a Primary Rooibos Flavonoid, Alleviates Mast Cell-Mediated Allergic Inflammation by the Inhibition of FcεRI Signaling Pathway.

Mast cells are primary cells initiating allergic inflammation by the release of various allergic mediators, such as histamine and pro-inflammatory cytokines. Aspalathin (ASP) is the predominant flavonoid found exclusively in rooibos, an herb that has been traditionally used in allergy relief therapy. In the present study, we investigated the beneficial effects of ASP on mast cell-mediated allergic inflammation. For in vivo study, two well-known mast cell-mediated local and systemic allergic inflammation mouse models were used: passive cutaneous anaphylaxis (PCA) and active systemic anaphylaxis mouse models (ASA). Oral administration of ASP dose-dependently suppressed immunoglobulin (Ig)E-mediated PCA responses evidenced by Evans blue extravasation, ear thickening, and mast cell degranulation. ASP also significantly mitigated ovalbumin-induced ASA responses, including hypothermia, histamine secretion, and the production of IgE and interleukin-4. Notably, ASP was more effective in suppressing allergic inflammation than nothofagin, another prominent flavonoid known as an anti-allergic component of rooibos. The regulatory mechanism of mast cell activation by ASP was clarified using mast cell line and primary cultured mast cells (RBL-2H3 and mouse bone marrow-derived mast cells). ASP reduced IgE-stimulated mast cells degranulation and intracellular calcium influx by the inhibition of FcεRI signaling pathway (Lyn, Fyn, and Syk). Moreover, ASP reduced pro-inflammatory cytokine expressions by inhibiting two major transcription factors, nuclear factor of activated T cells and nuclear factor-κB. Collectively, we proposed that ASP could be a potential therapeutic candidate for the treatment of mast cell-mediated allergic inflammatory diseases.

Targeted Single Particle Tracking with Upconverting Nanoparticles.

Single particle tracking (SPT) is a powerful technique for real-time microscopic visualization of the movement of individual biomolecules within or on the surface of living cells. However, SPT often suffers from the suboptimal performance of the photon-emitting labels used to tag the biomolecules of interest. For example, fluorescent dyes have poor photostability, while quantum dots suffer from blinking that hampers track acquisition and interpretation. Upconverting nanoparticles (UCNPs) have recently emerged as a promising anti-Stokes luminescent label for SPT. In this work, we demonstrated targeted SPT using UCNPs. For this, we synthesized 30 nm diameter doped UCNPs and coated them with amphiphilic polymers decorated with polyethylene glycol chains to make them water-dispersible and minimize their nonspecific interactions with cells. Coated UCNPs highly homogeneous in brightness (as confirmed by a single particle investigation) were functionalized by immunoglobulin E (IgE) using a biotin-streptavidin strategy. Using these IgE-UCNP SPT labels, we tracked high-affinity IgE receptors (FcεRI) on the membrane of living RBL-2H3 mast cells at 37 °C in the presence and absence of antigen and obtained good agreement with the literature. Moreover, we used the FcεRI-IgE receptor-antibody system to directly compare the performance of UCNP-based SPT labels to organic dyes (AlexaFluor647) and quantum dots (QD655). Due to their photostability as well as their backgroundless and continuous luminescence, SPT trajectories obtained with UCNP labels are no longer limited by the photophysics of the label but only by the dynamics of the system and, in particular, the movement of the label out of the field of view and/or focal plane.

EFFECT OF 4-(TRIFLUOROMETHOXY)PHENYLHYDRAZONE CARBONYL CYANIDE (FCCP) ON FCΕRI-DEPENDENT CYTOKINE PRODUCTION BY RBL-2H3 CELLS

Mast cells (MCs) play a key role in the development of allergic diseases. The interaction of antigens with immunoglobulin E and the subsequent binding of these complexes to the FcεRI receptor, which ultimately leads to rapid exocytosis of granules and subsequent production of cytokines, play a major role in MC activation in allergy. There is data on the role of the mitochondrial membrane potential in the FcεRI-dependent activation of MC. Thus, the use of classical uncouplers of oxidative phosphorylation reduces MC degranulation. However, their e ect on the production of MC cytokines has not been studied. In the present work, it was demonstrated that pretreatment of RBL-2H3 mast cells with the uncoupler carbonyl cyanide-4-(tri uoromethoxy)phenylhydrazone (FCCP) leads to a decrease not only in FcεRI-dependent degranulation, but also in a decrease in the production of TNFα and IL-4 cytokines. At the same time, FCCP prevents the phosphorylation of the LAT adapter molecule, as well as the Erk1/2 kinase, which may underlie the inhibitory e ect of the uncoupler on FcεRI-dependent activation of RBL-2H3 cell line. The data obtained indicate that the mitochondrial membrane potential plays an important role in the FcεRI-dependent activation of MC, and the uncoupling of oxidative phosphorylation and respiration of mitochondria with the help of uncouplers can be used to regulate this process.

Alisol B 23-Acetate Ameliorates Ovalbumin-Induced Allergic Asthma during Sensitization and Challenge Periods.

Rhizome of Alisma orientale has been used as a traditional medicine for treating kidney diseases in East Asian countries. Its inhibitory effects on hypersensitivity responses have been reported for methanol extracts, with alisol B 23-acetate (AB23Ac) being the most active constituent among six terpenes in inhibiting the direct passive Arthus reaction. However, whether AB23Ac has efficacy against allergic asthma has not been tested to date. The in vivo efficacy of AB23Ac in an ovalbumin (OVA)-induced allergic asthma mouse model was evaluated by administrating AB23Ac before OVA sensitization or OVA challenge in BALB/c mice. AB23Ac suppressed antigen-induced degranulation of RBL-2H3 mast cells in a concentration-dependent manner. The administration of AB23Ac both before OVA sensitization and OVA challenge greatly lowered pulmonary resistance and the increase in immune cell counts and inflammatory responses around the peribronchial and perivascular regions. In addition, the inflammatory cytokine levels of Th1/Th2/Th17 cells in the bronchoalveolar lavage fluid decreased in the AB23Ac-treated groups. AB23Ac reduced the number of PAS-stained cells in the lungs. Furthermore, a computer modeling study indicated that AB23Ac can bind tightly to spleen tyrosine kinase (Syk). These results suggest that AB23Ac may ameliorate allergic asthma by suppressing immune responses in dendritic cells during sensitization and in mast cells during challenge periods.

Exocytic machineries differentially control mediator release from allergen-triggered RBL-2H3 cells.

Mast cells utilize SNAREs (soluble-N-ethyl-maleimide sensitive factor attachment protein receptors) and SM (Sec1/Munc18) proteins to secrete/exocytose a variety of proinflammatory mediators. However, whether a common SNARE-SM machinery is responsible remains unclear. Four vesicle/granule-anchored SNAREs (VAMP2, VAMP3, VAMP7, and VAMP8) and two Munc18 homologs (Munc18a and Munc18b) were systematically knocked down or knocked out in RBL-2H3 mast cells and antigen-induced release of β-hexosaminidase, histamine, serotonin, and TNF was examined. Phenotypes were validated by rescue experiments. Immunofluorescence studies were performed to determine the subcellular distribution of key players. The reduction of VAMP8 expression inhibited the exocytosis of β-hexosaminidase, histamine, and serotonin but not TNF. Unexpectedly, however, confocal microscopy revealed substantial co-localization between VAMP8 and TNF, and between TNF and serotonin. Meanwhile, the depletion of other VAMPs, including knockout of VAMP3, had no impact on the release of any of the mediators examined. On the other hand, TNF exocytosis was diminished specifically in stable Munc18bknockdown cells, in a fashion that was rescued by exogenous, RNAi-resistant Munc18b. In line with this, TNF was co-localized with Munc18b (47%) to a much greater extent than with Munc18a (13%). Distinct exocytic pathways exist in mast cells for the release of different mediators.

Photopharmacological dissociation of transcriptional activation and degranulation of mast cells.

Besides a key role in allergic diseases, mast cells confer important modulatory functions in innate and adaptive immunity. The communication between mast cells and other immune cells is not only based on the acute or long-term release of pre-stored mediators involving distinct processes of degranulation but also on the expression of specific surface proteins. Activation of mast cells typically involves Ca2+ signalling, which evokes both transcriptional activation and degranulation. To dissect the complex functions of mast cells in human pathology and to explore new therapeutic strategies we aimed towards specific manipulation of mast cell phenotype. Characterization of an optochemogenetic protocol for activation RBL-2H3 mast cells revealed that repetitive photocycling of OptoBI-1 to generate oscillatory Ca2+ signals elicits rapid and efficient NFAT nuclear translocation without concomitant degranulation. By contrast, conventional pharmacological activation of overexpressed TRPC6 channel was strictly associated with CD63-associated secretion. Our results suggest that the specific modulation of mast cell phenotype as obtained by TRPC6-OptoBI-1-mediated activation, arises from introduction of a highly specific conformational and functional state of the TRPC6 channel, resulting in unique Ca2+signatures. Further understanding of these phenomena may lead to new approaches for (photo)pharmacological immunomodulation.

Insight into the conformational and allergenicity alterations of shrimp tropomyosin induced by Sargassum fusiforme polyphenol

Tropomyosin (TM) is the main allergen in shrimp food. Algae polyphenol reportedly could affect the structures and allergenicity of shrimp TM. In this study, the alterations of conformational structures and allergenicity of TM induced by Sargassum fusiforme polyphenol (SFP) were investigated. Compared to TM, the conjugation of SFP to TM induced conformational structure instability, the IgG-binding capacity and IgE-binding capacity of TM gradually decreased with more conjugation of SFP to TM, and the conjugation of SFP to TM could significantly reduce degranulation, histamine secretion and release of IL-4 and IL-13 from RBL-2H3 mast cells. Therefore, the conjugation of SFP to TM led to conformational instability, significantly decreased the IgG-binding capacity and IgE-binding capacity, weakened the allergic responses of TM-stimulated mast cell, and performed in vivo anti-allergic properties in BALB/c mouse model. Therefore, SFP could serve as candidate natural anti-allergic substances to reduce shrimp TM-induced food allergy.

Amber Extract Suppressed Mast Cell-Mediated Allergic Inflammation via the Regulation of Allergic Mediators—An In Vitro Study

The various clinical approaches for treating allergy-related diseases have shown modest progress in low side effects and improved clinical outcomes. Therefore, finding alternative anti-allergic agents is crucial. The present study explored the anti-allergic effects of amber extract (fossilized tree resin) in RBL-2H3 mast cells stimulated with different allergens. In order to support the information on the inflammatory effect of the amber extract, NO production analysis on RAW 264.7 cells was conducted. β-Hexosaminidase release, an indicator of the efficacy of the amber extract in preventing mast cell activation and degranulation, reactive oxygen species (ROS) generation, and the effect of the amber extract on key cytokines production on RBL-2H3 cells, was evaluated. The results demonstrated that amber extract at concentrations up to 50 μg/mL had no cytotoxic effect on RAW 264.7 and RBL-2H3 cells. Amber extract inhibited NO production in RAW 264.7 cells. Treatment with amber extract significantly suppressed the release of β-hexosaminidase, especially at 50 μg/mL. Furthermore, amber extract suppressed the significantly increased ROS levels induced by allergen stimulation and allergy-associated cytokines. The results also suggested that amber extract exerts anti-allergic inflammatory effects by inhibiting the MAPK and NF-κB signaling pathways, resulting in decreased cytokines production. Thus, the amber extract is a promising anti-allergic agent.

360 TLR4 Plays An Important Role In Chronic Relapsing Pruritus Induced By Subcutaneous Capsaicin Injection In Neonatal Rats

Despite the high prevalence of chronic dermatitis and the accompanied intractable itch, therapeutics that specifically target itching have low efficacy. Although toll-like receptors (TLRs) are suggested to contribute to immune activation and neural sensitization, their roles in chronic itch in the skin remain elusive. Here, we show that the RBL-2H3 mast cell line expresses TLR4 and that treatment with a TLR4 antagonist opposes the LPS-dependent increase in mRNA levels of Th2 and innate cytokines.

RBL-2H3 Mast Cell Receptor Dynamics in the Immunological Synapse.

The RBL-2H3 mast cell immunological synapse dynamics is often simulated with reaction-diffusion and Fokker-Planck equations. The equations focus on how the cell synapse captures receptors following an immune response, where the receptor capture at the immunological site appears to be a delayed process. This article investigates the physical nature and mathematics behind such time-dependent delays. Using signal processing methods, convolution and cross-correlation-type delay capture simulations give a -squared range of 22 to 60, in good agreement with experimental results. The cell polarization event is offered as a possible explanation for these capture delays, where polarizing rates measure how fast the cell polarization event occurs. In the case of RBL-2H3 mast cells, polarization appears to be associated with cytoskeletal rearrangement; thus, both cytoskeletal and diffusional components are considered. From these simulations, a maximum polarizing rate ranging from 0.0057 s-2 to 0.031 s-2 is obtained. These results indicate that RBL-2H3 mast cells possess both temporal and spatial memory, and cell polarization is possibly linked to a Turing-type pattern formation.

Ameliorative Effects of Daphnopsis costaricensis Extract against Oxazolone-Induced Atopic Dermatitis-like Lesions in BALB/c Mice.

The genus Daphnopsis has been traditionally used as a purgative, diuretic, stimulant, and psoriasis treatment. In this study, the anti-AD (atopic dermatitis) activities of the Daphnopsis costaricensis EtOH extract (DCE) were investigated in an oxazolone (OX)-induced mouse model of AD, and the anti-inflammatory effects of its active compounds were confirmed in PI-sensitized or IgE/DNP-BSA-sensitized RBL-2H3 cells. DCE improved the symptoms of OX-induced inflammatory dermatitis (swelling, erythema, and increased ear thickening) in OX-induced BALB/c mice ears and reduced epidermal thickness and mast cell infiltration. Eleven flavonoid compounds were isolated from DCE, and two compounds (7,8-dimethoxyflavone and 7,2'-dimethoxyflavone) significantly inhibited IL-4 overexpression in PI-induced RBL-2H3 cells and mast cell degranulation in IgE + DNP-BSA-induced RBL-2H3 cells. Our study indicates that DCE and two compounds (7,8-dimethoxyflavone and 7,2'-dimethoxyflavone) might effectively improve inflammatory and atopic skin symptoms.

NJK14047 Suppression of the p38 MAPK Ameliorates OVA-Induced Allergic Asthma during Sensitization and Challenge Periods.

p38 MAPK has been implicated in the pathogenesis of asthma as well as pro-allergic Th2 cytokines, orosomucoid-like protein isoform 3 (ORMDL3), regulation of sphingolipid biosynthesis, and regulatory T cell-derived IL-35. To elucidate the role of p38 MAPK in the pathogenesis of asthma, we examined the effect of NJK14047, an inhibitor of p38 MAPK, against ovalbumin (OVA)-induced allergic asthma; we administrated NJK14047 before OVA sensitization or challenge in BALB/c mice. As ORMDL3 regulation of sphingolipid biosynthesis has been implicated in childhood asthma, ORMDL3 expression and sphingolipids contents were also analyzed. NJK14047 inhibited antigen-induced degranulation of RBL-2H3 mast cells. NJK14047 administration both before OVA sensitization and challenge strongly inhibited the increase in eosinophil and lymphocyte counts in the bronchoalveolar lavage fluid. In addition, NJK14047 administration inhibited the increase in the levels of Th2 cytokines. Moreover, NJK14047 reduced the inflammatory score and the number of periodic acid-Schiff-stained cells in the lungs. Further, OVA-induced increase in the levels of C16:0 and C24:1 ceramides was not altered by NJK14047. These results suggest that p38 MAPK plays crucial roles in activation of dendritic and mast cells during sensitization and challenge periods, but not in ORMDL3 and sphingolipid biosynthesis.

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

Mast cell activation plays a key role in various allergic diseases and anaphylaxis. Several methods/techniques can be used for detection of mast cell activation. However, there was no previous systematic evaluation to compare the efficacy of each method/technique. The present study thus systematically compared various markers for mast cell activation induced by IgE cross-linking. The widely used RBL-2H3 mast cells were sensitized with anti-DNP (dinitrophenyl) IgE overnight and activated with DNP-BSA (bovine serum albumin) for up to 4h. The untreated cells and those with anti-DNP IgE sensitization but without DNP-BSA activation served as the controls. Intracellular calcium level gradually increased to ~2-fold at 1h, reached its peak (~5-fold) at 2h, and returned to the basal level at 3-h post-activation. The increases in cellular tryptase level (by Western blotting) (~0.3- to 0.4-fold) and average cell size (~2.5-fold) and decrease of nucleus/cytoplasm ratio (~0.4- to 0.5-fold) were marginal at all time-points. By contrast, β-hexosaminidase release and CD63 expression (by both flow cytometry and immunofluorescence detection/localization), secreted tryptase level (by Western blotting), and tryptase expression (by immunofluorescence detection/localization) stably and obviously increased (~10-fold as compared with the untreated control and sensitized-only cells or detectable only after activation). Based on these data, the stably obvious increases (by ≥ 10-fold) in β-hexosaminidase release, CD63 expression (by both flow cytometry and immunofluorescence staining), secreted tryptase level (by Western blotting), and tryptase expression (by immunofluorescence staining) are recommended as the markers of choice for the in vitro study of mast cell activation using RBL-2H3 cells.

Docking of Syk to FcεRI is enhanced by Lyn but limited in duration by SHIP1.

The high-affinity immunoglobulin E (IgE) receptor, FcεRI, is the primary immune receptor found on mast cells and basophils. Signal initiation is classically attributed to phosphorylation of FcεRIβ-and γ-subunits by the Src family kinase (SFK) Lyn, followed by the recruitment and activation of the tyrosine kinase Syk. FcεRI signaling is tuned by the balance between Syk-driven positive signaling and the engagement of inhibitory molecules, including SHIP1. Here, we investigate the mechanistic contributions of Lyn, Syk, and SHIP1 to the formation of the FcεRI signalosome. Using Lyn-deficient RBL-2H3 mast cells, we found that another SFK can weakly monophosphorylate the γ-subunit, yet Syk still binds the incompletely phosphorylated immunoreceptor tyrosine-based activation motifs (ITAMs). Once recruited, Syk further enhances γ-phosphorylation to propagate signaling. In contrast, the loss of SHIP1 recruitment indicates that Lyn is required for phosphorylation of the β-subunit. We demonstrate two noncanonical Syk binding modes, trans γ-bridging and direct β-binding, that can support signaling when SHIP1 is absent. Using single particle tracking, we reveal a novel role of SHIP1 in regulating Syk activity, where the presence of SHIP1 in the signaling complex acts to increase the Syk:receptor off-rate. These data suggest that the composition and dynamics of the signalosome modulate immunoreceptor signaling activities.

518 Role Of TLR4 In chronic relapsing itch induced by subcutaneous capsaicin injection in neonatal rats

Despite the high prevalence of chronic dermatitis and the accompanied intractable itch, therapeutics that specifically target itching have low efficacy. Increasing evidence suggests that TLRs contribute to immune activation and neural sensitization; however, their roles in chronic itch remain elusive. Here, we show that the RBL-2H3 mast cell line expresses TLR4 and that treatment with a TLR4 antagonist opposes the LPS dependent increase in mRNA levels of Th2 and innate cytokines. The pathological role of TLR4 activation in itching was studied in neonate rats that developed chronic itch due to neuronal damage after receiving subcutaneous capsaicin injections.

Lactobacillus gasseri MG4247 and Lacticaseibacillus paracasei MG4272 and MG4577 Modulate Allergic Inflammatory Response in RAW 264.7 and RBL-2H3 cells.

Allergic inflammation refers to a hyperimmune reaction that causes hypersensitivity responses such as hives, itchiness, runny nose, and cough due to specific allergens. Allergic diseases are known to be influenced by the diversity and distribution of intestinal microbiota, and Lactobacill is known to relieve allergic symptoms by modulating cytokines secreted by T helper type 1 (Th1)/Th2 cells. This study was designed to investigate the effects of Lactobacillus gasseri MG4247 and Lacticaseibacillus paracasei MG4272, MG4577, and MG4657 on levels of pro-inflammatory cytokines and proteins associated with allergic symptoms in RAW 264.7 macrophages, and RBL-2H3 mast cells, as well as their probiotic properties. MG4247, MG4272, and MG4577 significantly reduced tumor necrosis factor-α and interleukin (IL)-6 levels in LPS-induced RAW 264.7 macrophages, and markedly decreased IL-4, IL-5, and IL-13 levels and STAT6 phosphorylation in DNP-IgE/HSA sensitized RBL-2H3 mast cells. Furthermore, MG4247, MG4272, and MG4577 tolerated the acidic condition with pepsin and basic condition with bile salt, and showed a high adhesion rate (≥ 73.9%). In safety evaluation, MG4247, MG4272, and MG4577 showed no hemolytic or bile salt hydrolase activity and no cytotoxicity to HT-29 cells (≥ 96.7%). Hence, MG4272, MG4272, and MG4577 can be used as candidate probiotic strains to relieve cytokines associated with allergic inflammation. Supplementary InformationThe online version contains supplementary material available at 10.1007/s12602-022-09950-4.

유산균 발효 양배추의 생리활성 특성

White cabbage (Brassica oleracea var. capitata) reportedly exerts antioxidant, anti-inflammatory, and anti-gastric effects. We aimed to evaluate the biological activity of B. oleracea fermented with Lactobacillus plantarum (FBO). The plant material was fermented for 7 d. The antioxidative potentials of FBO (DPPH radical-scavenging activity, and total phenol and total flavonoid contents) and ability of FBO to inhibit digestive enzymes (α-amylase and lipase) were tested. Anti-inflammatory and anti-allergic effects were also determined by measuring the release of NO, inflammatory cytokines (IL-1β, TNF-α and IL-4), β-hexosaminidase and histamine. FBO contained 15.84±0.25 mg GAE/g phenols and 1.19±0.09 mg NA/g flavonoids. FBO showed DPPH radical-scavenging activity, and inhibited α-amylase and lipase. It also inhibited of NO, PGE2 and inflammatory cytokine production by LPS-stimulated RAW 264.7 macrophages. Finally, FBO inhibited degranulation and inflammatory cytokine production in antigen-stimulated RBL-2H3 mast cells, in a dose-dependent manner. Collectively, these observations indicate that white cabbage fermented with L. plantarum can be used as a functional material and edible resource in industrial setting.