lignans and Hypersensitivity

Topics: Asthma; Biomechanical Phenomena; Bronchial Provocation Tests; Bronchial Spasm; Bronchitis; Byssinosis; Cyanates; Dust; Edible Grain; Forecasting; Humans; Hypersensitivity; Insecticides; Lignans; Naphthols; Occupational Diseases; Organophosphorus Compounds; Prognosis; Reflex; Respiratory Function Tests; Respiratory Hypersensitivity; Serology; Skin Tests; Smoking; Terminology as Topic

Topics: Animals; Anti-Inflammatory Agents; Antineoplastic Agents, Phytogenic; Asthma; Cyclooctanes; Dendritic Cells; Disease Models, Animal; Forkhead Transcription Factors; Heme Oxygenase-1; Hypersensitivity; Immunoglobulin E; Immunomodulating Agents; Lignans; Mice; Mice, Inbred BALB C; Polycyclic Compounds; Respiratory Hypersensitivity; T-Lymphocytes, Regulatory; Th2 Cells

Topics: Animals; Anti-Allergic Agents; Biomarkers; Cell Line, Tumor; Chromatography, High Pressure Liquid; Glucosides; Histamine Antagonists; Hydrolyzable Tannins; Hypersensitivity; Ketotifen; Lignans; Mast Cells; Phyllanthus; Plant Extracts; Rats; Receptors, Histamine

We established a mouse model of allergic asthma by sensitizing with chicken ovalbumin. The volatile oils and decoctions from raw, wine- and vinegar-steamed Schisandra chinensis fruits were intragastrically administrated to the mice. Atomization, serum IgE, IL-2, IL-4 and IFN-γ in the lung homogenates and pathological sections were evaluated to compare the effect of these volatile oils and decoctions on allergic asthma in mice. The results showed that all Schisandra volatile oils could significantly suppress allergic asthma in mice. Raw Schisandra volatile oil was most effective followed by volatile oils extracted from wine-steamed and vinegar-steamed Schisandra. The decoctions had no significant impact. Our findings demonstrated that volatile oil was the active ingredient in Schisandra, and raw Schisandra could be used to prevent cough and asthma.

Topics: Animals; Asthma; Cyclooctanes; Fruit; Hypersensitivity; Lignans; Male; Mice; Oils, Volatile; Ovalbumin; Plant Extracts; Polycyclic Compounds; Schisandra

Mast cells (MCs) play critical roles in allergic reactions and modulating the activation of MCs could be an effective strategy to treat allergic diseases, which cause a rapidly increasing threat to the public health. Herein, we described that Magnolin, a major component from Flos magnoliae could inhibit IgE-dependent MCs activation. We found Magnolin inhibited IgE/Ag-induced calcium mobilization, degranulation, and cytokines release in LAD2 cells. Magnolin was also found to attenuate IgE/Ag-induced mice paw swelling in a dose-dependent manner. Further mechanistic studies suggested a possible anti-allergic and anti-inflammatory effects of Magnolin in IgE/Ag-induced anaphylactic reactions. Thereby, Magnolin could be a potential therapeutic agent for preventing mast cell-related immediate and delayed allergic diseases.

Topics: Anaphylaxis; Animals; Anti-Allergic Agents; Antigens; Calcium; Cell Line; Cell Survival; Cytokines; Edema; Histamine; Humans; Hypersensitivity; Immunoglobulin E; Lignans; Male; Mast Cells; Mice, Inbred BALB C; Mitogen-Activated Protein Kinases; Peptide Hydrolases

Schisandra chinensis (SC) and its main constituent, schizandrin (SCH) exhibit anti-inflammatory and anti-allergic activities. Allergic and inflammatory reactions are aggravated via caspase-1 signaling pathway. However, the regulatory effects of SC and SCH on caspase-1 activation have not been clarified yet. In this study, we aimed to clarify the anti-allergic effects of SC and SCH using an ovalbumin (OVA)-sensitized mice and anti-CD3 and anti-CD28 antibodies-stimulated splenocytes. SC or SCH significantly inhibited the levels of immunoglobulin (Ig)E, IgG1, or interleukin (IL)-4 in serum of OVA-sensitized mice. SC or SCH significantly inhibited the levels of IL-6, tumor necrosis factor (TNF)-[Formula: see text], and IL-1[Formula: see text] in spleen of the OVA-sensitized mice. SC or SCH significantly suppressed the expression of caspase-1 and receptor-interacting protein (RIP)-2 in spleen of the OVA-sensitized mice. In activated splenocytes, SC or SCH significantly decreased the expression of caspase-1 and RIP-2 as well as the production of IL-6 and TNF-[Formula: see text]. We suggest that SC and SCH exert an anti-allergic effect by down-regulating caspase-1 signaling.

Topics: Animals; Caspase 1; Cyclooctanes; Down-Regulation; Hypersensitivity; Immunoglobulin E; Immunoglobulin G; Interleukin-1beta; Interleukin-4; Interleukin-6; Lignans; Mice; Ovalbumin; Plant Extracts; Polycyclic Compounds; Receptor-Interacting Protein Serine-Threonine Kinase 2; Receptor-Interacting Protein Serine-Threonine Kinases; Schisandra; Spleen; Tumor Necrosis Factor-alpha

Establishing therapeutic agents for the treatment of allergic diseases is an important focus of human health research. Sesamin, a lignan in sesame oil, exhibits a diverse range of pharmacological properties. However, to the best of our knowledge, the effect of sesamin on mast cell‑mediated allergic responses has not yet been investigated. Thus, the aim of the present study was to investigate the effect of sesamin on mast cell‑mediated allergic responses and the underlying mechanisms by which it produces this effect. In rats, oral administration of sesamin inhibited passive cutaneous anaphylaxis. Sesamin exposure attenuated immunoglobulin E‑induced histamine release from rat peritoneal mast cells, which was indicated to be mediated by the modulation of intracellular calcium. In human mast cells, sesamin reduced the stimulatory effects of phorbol 12‑myristate 13‑acetate and calcium ionophore A23187 on the production and secretion of pro‑inflammatory cytokines, including tumor necrosis factor‑α and interleukin‑6. The inhibitory effect of sesamin on pro‑inflammatory cytokine production was dependent on nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB) and p38 mitogen‑activated protein kinase (MAPK). The present study demonstrates that sesamin inhibits mast cell‑derived inflammatory allergic reactions by blocking histamine release, and pro‑inflammatory cytokine production and secretion. In addition, the findings indicate that the effect of sesamin is mediated by its effect on p38 MAPK/NF‑κB signaling. Furthermore, the in vivo and in vitro anti‑allergic effects of sesamin reported in the present study suggest that it is a promising therapeutic agent for the treatment of inflammatory allergic diseases.

Topics: 2,4-Dinitrophenol; Animals; Calcium; Cell Line; Cell Survival; Cytokines; Dioxoles; Enzyme Activation; Histamine Release; Humans; Hypersensitivity; Immunoglobulin E; Inflammation Mediators; Lignans; Male; Mast Cells; Mice, Inbred ICR; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Passive Cutaneous Anaphylaxis; Peritoneum; Rats, Sprague-Dawley

The present study aimed at developing a natural compound with anti-allergic effect and stability under latex glove manufacturing conditions and investigating whether its anti-allergic effect is maintained after its addition into the latex. The effects of nine natural compounds on growth of the RBL-2H3 cells and mouse primary spleen lymphocytes were determined using MTT assay. The compounds included glycyrrhizin, osthole, tetrandrine, tea polyphenol, catechin, arctigenin, oleanolic acid, baicalin and oxymatrine. An ELISA assay was used for the in vitro anti-type I/IV allergy screening; in this process β-hexosaminidase, histamine, and IL-4 released from RBL-2H3 cell lines and IFN-γ and IL-2 released from mouse primary spleen lymphocytes were taken as screening indices. The physical stability of eight natural compounds and the dissolubility of arctigenin, selected based on the in vitro pharnacodynamaic screening and the stability evaluation, were detected by HPLC. The in vivo pharmacodynamic confirmation of arctigenin and final latex product was evaluated with a passive cutaneous anaphylaxis (PCA) model and an allergen-specific skin response model. Nine natural compounds showed minor growth inhibition on RBL-2H3 cells and mouse primary spleen lymphocytes. Baicalin and arctigenin had the best anti-type I and IV allergic effects among the natural compounds based on the in vitro pharmacodynamic screening. Arctigenin and catechin had the best physical stability under different manufacturing conditions. Arctigenin was the selected for further evaluation and proven to have anti-type I and IV allergic effects in vivo in a dose-dependent manner. The final product of the arctigenin-containing latex glove had anti-type I and IV allergic effects in vivo which were mainly attributed to arctigenin as proved from the dissolubility results. Arctigenin showed anti-type I and IV allergic effects in vitro and in vivo, with a good stability under latex glove manufacturing conditions, and a persistent anti-allergic effect after being added into the latex to prevent latex allergy.

Topics: Animals; Anti-Allergic Agents; Biological Products; Cell Line; Cell Survival; Furans; Hypersensitivity; Hypersensitivity, Delayed; Hypersensitivity, Immediate; Latex; Latex Hypersensitivity; Lignans; Lymphocytes; Mice; Mice, Inbred BALB C

Type I allergy is characterized by the release of granule-associated mediators, lipid-derived substances, cytokines, and chemokines by activated mast cells. To evaluate the anti-allergic effects of macelignan isolated from Myristica fragrans Houtt., we determined its ability to inhibit calcium (Ca(2+)) influx, degranulation, and inflammatory mediator production in RBL-2 H3 cells stimulated with A23187 and phorbol 12-myristate 13-acetate. Macelignan inhibited Ca(2+) influx and the secretion of β-hexosaminidase, histamine, prostaglandin E(2), and leukotriene C(4); decreased mRNA levels of cyclooxygenase-2, 5-lipoxygenase, interleukin-4 (IL-4), IL-13, and tumor necrosis factor-α; and attenuated phosphorylation of Akt and the mitogen-activated protein kinases extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase. These results indicate the potential of macelignan as a type I allergy treatment.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Arachidonate 5-Lipoxygenase; beta-N-Acetylhexosaminidases; Calcimycin; Calcium; Cell Degranulation; Cell Line, Tumor; Cyclooxygenase 2; Dinoprostone; Extracellular Signal-Regulated MAP Kinases; Histamine Release; Hypersensitivity; Inflammation Mediators; Interleukin-13; Interleukin-4; JNK Mitogen-Activated Protein Kinases; Leukemia, Basophilic, Acute; Leukotriene C4; Lignans; Mast Cells; Myristica; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Plant Extracts; Proto-Oncogene Proteins c-akt; Rats; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha

Gomisin N is a bioactive compound and a prominent anti-allergic agent found in the fruits of tree Schizandra chinensis. However, its effects on the bone marrow-derived mast cell (BMMC)-mediated allergy and inflammation mechanism remain unknown. In this study, the biological effects of gomisin were evaluated while focusing on its effects on the allergic mediator in PMA + A23187-stimulated BMMCs. The anti-allergic effect of gomisin has shown that inhibited PMA + A23187-induced interleukin-6 (IL-6) production. An investigation was also conducted to determine its effects on the production of several allergic mediators including prostaglandin D(2) (PGD(2)), leukotriene C(4) (LTC(4)), β-hexosaminidase (β-Hex), and cyclooxygenase-2 (COX-2) protein. The results revealed that gomisin inhibited the PMA + A23187-induced production of IL-6, PGD(2), LTC(4), β-Hex, and COX-2 protein. Taken together, these findings indicate that gomisin N has the potential for use in the treatment of allergy.

Topics: Animals; Anti-Allergic Agents; Bone Marrow Cells; Calcimycin; Calcium Ionophores; Carcinogens; Cells, Cultured; Cyclooctanes; Gene Expression Regulation; Hypersensitivity; Inflammation; Inflammation Mediators; Interleukin-6; Lignans; Male; Mast Cells; Mice; Mice, Inbred BALB C; Polycyclic Compounds; Tetradecanoylphorbol Acetate

We previously reported that arctigenin, a phenylpropanoid dibenzylbutyrolactone lignan isolated from Forsythia koreana, exhibits anti-inflammatory, antioxidant, and analgesic effects in animal models. In addition, arctigenin inhibited eosinophil peroxidase and activated myeloperoxidase in inflamed tissues. In this study, we tested the effects of arctigenin on type I-IV allergic inflammation and pro-inflammatory enzymes in vitro and in vivo. Arctigenin significantly inhibited the heterologous passive cutaneous anaphylaxis induced by ovalbumin in mice at 15 mg/kg, p.o., and compound 48/80-induced histamine release from rat peritoneal mast cells at 10 microM. Arctigenin (15 mg/kg, p.o.) significantly inhibited reversed cutaneous anaphylaxis. Further, arctigenin (15 mg/kg, p.o.) significantly inhibited the Arthus reaction to sheep's red blood cells, decreasing the hemolysis titer, the hemagglutination titer, and the plaque-forming cell number for SRBCs. In addition, arctigenin significantly inhibited delayed type hypersensitivity at 15 mg/kg, p.o. and the formation of rosette-forming cells at 45 mg/kg, p.o. Contact dermatitis induced by picrylchloride and dinitrofluorobenzene was significantly (p < 0.05) inhibited by surface treatment with arctigenin (0.3 mg/ear). Furthermore, arctigenin dose-dependently inhibited pro-inflammatory enzymes, such as cyclooxygenase-1 and 2, 5-lipoxygenase, phospholipase A2, and phosphodiesterase. Our results show that arctigenin significantly inhibited B- and T-cell mediated allergic inflammation as well as pro-inflammatory enzymes.

Topics: Animals; Anti-Allergic Agents; Anti-Inflammatory Agents, Non-Steroidal; B-Lymphocytes; Enzyme Inhibitors; Furans; Guinea Pigs; Hemagglutination; Histamine Antagonists; Histamine Release; Hypersensitivity; Inflammation; Lignans; Lung; Male; Mast Cells; Mice; Mice, Inbred BALB C; Rats; Rats, Sprague-Dawley; Skin; T-Lymphocytes

Chronic airway inflammation is a hallmark of asthma, an immune-based disease with great societal impact. Honokiol (HNK), a phenolic neurotransmitter receptor (γ-aminobutyric acid type A) agonist purified from magnolia, has anti-inflammatory properties, including stabilization of inflammation in experimentally induced arthritis. The present study tested the prediction that HNK could inhibit the chronic inflammatory component of allergic asthma. C57BL/6 mice sensitized to and challenged with OVA had increased airway hyperresponsiveness to methacholine challenge and eosinophilia compared with naive controls. HNK-treated mice showed a reduction in airway hyperresponsiveness as well as a significant decrease in lung eosinophilia. Histopathology studies revealed a marked drop in lung inflammation, goblet cell hyperplasia, and collagen deposition with HNK treatment. Ag recall responses from HNK-treated mice showed decreased proinflammatory cytokines in response to OVA, including TNF-α-, IL-6-, Th1-, and Th17-type cytokines, despite an increase in Th2-type cytokines. Regulatory cytokines IL-10 and TGF-β were also increased. Assessment of lung homogenates revealed a similar pattern of cytokines, with a noted increase in the number of FoxP3(+) cells in the lung. HNK was able to alter B and T lymphocyte cytokine secretion in a γ-aminobutyric acid type A-dependent manner. These results indicate that symptoms and pathology of asthma can be alleviated even in the presence of increased Th2 cytokines and that neurotransmitter agonists such as HNK have promise as a novel class of anti-inflammatory agents in the treatment of chronic asthma.

Topics: Animals; Anti-Inflammatory Agents; Asthma; Biphenyl Compounds; Cytokines; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Eosinophilia; Female; Fluorescent Antibody Technique; Hypersensitivity; Lignans; Lung; Mice; Mice, Inbred C57BL; Th2 Cells

Occupational asthma due to western red cedar is associated with histamine release from basophils and mast cells on exposure to plicatic acid (PA), but the mechanisms underlying this response remain unclear. Specific kinase inhibitors were used to study the role of tyrosine and serine/threonine kinases in PA-induced histamine release from human basophils. Pretreatment with the tyrosine kinase inhibitor methyl 2,5-dihydroxy-cinnamate (MDHC) attenuated histamine release from basophils triggered by anti-IgE (29.8% inhibition; n = 15; P < 0.01) or grass pollen (48% inhibition; n = 6; P < 0.01). Inhibition was concentration-dependent and could be reversed by washing the cells in buffer, while the inactive stereoisomer of MDHC did not affect histamine release. In contrast, the protein kinase C inhibitor staurosporine did not affect histamine release by either anti-IgE or grass pollen. Pretreatment with MDHC partially inhibited PA-induced histamine release from basophils of 6/9 patients with red cedar asthma (25.4% vs 33.8%; P = NS). Staurosporine gave a similar level of inhibition of PA-induced histamine release (25.3% vs 33.8%; P = NS). Thus, signal transduction of the human basophil Fc epsilon RI appears to depend upon tyrosine kinase activation, but not on protein kinase C (serine/threonine kinase) activation. The lack of specific effect on plicatic acid-induced histamine release in basophils obtained from patients with occupational asthma due to western red cedar suggests that tyrosine kinases are not as important in this disease as in atopic asthma, and is consistent with the view that histamine release in red cedar asthma is largely IgE-independent.

Topics: Allergens; Antibodies, Anti-Idiotypic; Asthma; Basophils; Cinnamates; Environmental Exposure; Enzyme Activation; Enzyme Inhibitors; Histamine; Histamine Antagonists; Humans; Hypersensitivity; Lignans; Naphthols; Poaceae; Pollen; Protein-Tyrosine Kinases; Trees

It is unknown whether factors such as the nature of the agent, gender, age, atopy, smoking habits, continuous or noncontinuous exposure, and pattern of asthmatic reaction can influence the rate of development of symptoms in subjects with occupational asthma. We compared several clinical and functional parameters among three groups of subjects with occupational asthma caused by Western red cedar (group 1, n = 433), isocyanates (group 2, n = 107), and high molecular weight agents acting through an IgE-mediated mechanism (group 3, n = 121). Survival analysis showed that the three curves relating years of exposure before onset of symptoms to the proportion of subjects without symptoms were significantly different in two respects: (1) almost 40% of subjects in groups 1 and 2 as compared with 20% of subjects in group 3 became symptomatic within 1 year of exposure; (2) after 5 years of exposure, the rate of sensitization was slower for subjects in groups 2 and 3 as compared with those in group 1. Having a nonimmediate reaction at the time of specific inhalation challenges, being continuously exposed and being younger slightly increased the risk at each time point on the curve of developing symptoms in subjects with occupational asthma. These data suggest that the natural history for onset of occupational asthma is different depending on the sensitizing agent. Factors such as age, type of exposure, and pattern of reaction on exposure to the agent also modulate the rate of development of this condition.

Topics: Adult; Allergens; Asthma; Cyanates; Female; Forced Expiratory Volume; Humans; Hypersensitivity; Hypersensitivity, Immediate; Lignans; Male; Middle Aged; Molecular Weight; Naphthols; Occupational Diseases; Smoking

Topics: Guaiac; Guaiacol; Humans; Hypersensitivity; Lignans