We aimed to evaluate the anti-allergic effect of luteolin treatment in mice with allergic asthma and rhinitis.Thirty-two BALB/c mice (n = 8 for each group) were used. Mice in group A (nonallergic group) were exposed to saline, while those in Group B (allergic group) were exposed to ovalbumin (OVA) intraperitoneal (i.p.) injection and intranasal (i.n.) challenge. Null treatment group (Group C) received sterile saline (150 μl) i.p. injection, 30 minutes before each i.n. challenge. Finally, the treatment group (Group D) received luteolin (0.1 mg/kg) by i.p. injection, 30 minutes before each i.n. challenge. We evaluated the number of inflammatory cells including eosinophils, neutrophils and lymphocytes in bronchoalveolar lavage (BAL) fluid, the titers of IL-4, IL-5 and IL-13 in lung homogenate, and we also evaluated histopathologic findings, including infiltration of inflammatory cells into the pulmonary parenchyma and nasal mucosa.After the OVA challenge, the number of eosinophils, neutrophils and lymphocytes in BAL fluid was significantly increased in group B, compared to group A (p < 0.001). Mice in group C had no significant difference (p > 0.05). On the other hand, group D showed a significant decrease in all inflammatory cells compared to group B (p < 0.05). Also, group D showed a significant decrease in IL-4, IL-5 and IL-13 in their lung homogenate compared to groups B and C (p < 0.05). Group D also showed a significant decrease in inflammatory cell infiltration after luteolin treatment (p < 0.05).Luteolin had an anti-allergic effect in a murine model of allergic asthma and rhinitis.
Background Glucosamine (GlcN) is generally used as a dietary supplement because of its antiinflammatory effects. We evaluated the antiallergic effect of GlcN in mice with allergic asthma and rhinitis. Methods Thirty‐two mice were allocated equally into 4 groups (n = 8). In group A (control), we performed intraperitoneal/intranasal challenge using sterile saline. In group B (asthma/rhinitis), we used ovalbumin for intraperitoneal/intranasal challenge to induce allergic asthma and rhinitis. In groups C and D (GlcN treatment), mice were given 1% and 5% GlcN throughout the period of ovalbumin challenge, respectively. We measured serum total and ovalbumin‐specific immunoglobulin E (IgE), cytokine titers (interleukin‐1, ‐4, ‐5, ‐6, ‐10, and ‐17; tumor necrosis factor‐α; and interferon‐γ), and the number of inflammatory cells (eosinophils, neutrophils, lymphocytes) in bronchoalveolar lavage (BAL) fluid. We also performed histopathologic examination of the lung and nasal cavity. Finally, we performed real‐time polymerase chain reaction for the genes Bcl‐2 , EC‐SOD , VEGF , caspase‐3 , Bax , COX‐2 , Hif‐1α , and heme oxygenase‐1 . Results Compared with group B, group D had significant serum total and ovalbumin‐specific IgE decreases after GlcN treatment ( p < 0.05). Titers for IL‐4, IL‐5, IL‐6, and IL‐17 in BAL fluid were significantly decreased in group D ( p < 0.05). Eosinophils in BAL fluid were significantly decreased in group D compared with group B ( p < 0.05). Groups C and D showed significant improvement of inflammation compared with group B. Group D had significant downregulation of EC‐SOD , Bax , Hif‐1α , and heme oxygenase‐1 compared with group B. Conclusion GlcN had a significant antiallergic effect in mice with allergic asthma and rhinitis.
We evaluated the effect of acute hypergravity (HG) on the immune response in a murine model of allergic asthma.Twenty-eight BALB/c mice were used. Group A (control group, n = 7) mice were sensitized and challenged with normal saline. Group B (control HG exposure group, n = 7) mice were sensitized, challenged with saline, and exposed to acute HG (+10 Gz) for 4 hours. Group C (asthma group, n = 7) mice were challenged with intraperitoneal and intranasal ovalbumin (OVA) to induce asthma. Group D (asthma HG exposure group, n = 7) mice were exposed to HG for 4 hours after the induction of asthma. We estimated the total and OVA-specific serum IgE, serum titers of various cytokines, and the number of eosinophils, neutrophils, and lymphocytes in bronchoalveolar lavage (BAL) fluid. Histopathology of the lung was also evaluated.The serum level of interleukin (IL)-5 was significantly higher in Group D (12.9 ±4.9 pg/ml) compared to that in Group C (4.7 ±6.5 pg/ml, p = 0.017). In BAL fluid, the number of neutrophils was significantly increased in Group D compared to Group C (p = 0.014). Group D demonstrated a higher infiltration of inflammatory cells (9973.8 ±1642.7 cells/mm(2)) compared to Group C (7666.3 ±586.5 cells/mm(2), p = 0.017). This tendency of increase in infiltration was not significant in non-asthmatic animals (Group A: 4488.8 ±176.1 cells/mm(2) vs. Group B: 4946.3 ±513.7 cells/mm(2), p > 0.05).Acute HG exacerbated the allergic response by increasing serum IL-5 levels and promoting pulmonary infiltration of inflammatory cells.
Objective We aimed to find novel genes that are significantly induced in allergic mice and that are significantly downregulated with anti-interleukin (IL) 33 treatment. Methods Thirty-six mice were allocated into each of group A (intraperitoneal [i.p.]) sensitized and intranasally challenged to saline solution), group B (sensitized and challenged to ovalbumin), group C (sensitized and challenged with ovalbumin, and null treatment with i.p. saline solution), and group D (sensitized and challenged with ovalbumin, and treatment with anti-IL-33 i.p. injection). We counted the number of nose-scratching in 10 minutes, serum ovalbumin-specific immunoglobulin E (IgE), and titers of cytokines (IL-1, IL-4, IL-5, IL-10, IL-13) in bronchoalveolar lavage fluid. By using one whole lung from each mouse, we performed microarray analysis and real-time polymerase chain reaction. Results Group D showed a significantly reduced nose-scratching events and lower serum ovalbumin-specific IgE compared with groups B and C. All the cytokines in the bronchoalveolar lavage fluid were significantly decreased after anti-IL-33 treatment. Microarray analysis revealed that group B (immunoglobulin free light chain [IgFLC], 89.1 times; nitric oxide synthase [NOS] 2,11.5 times) and group C (IgFLC, 141.6 times; NOS2,11.7 times) had significantly increased expression of IgFLC and NOS2 genes compared with group A. After anti-IL-33 treatment, group D showed significantly decreased expression of both IgFLC (49.3 times) and NOS2 (6.5 times). In real-time polymerase chain reaction, groups B and C had significantly increased expression of these genes (IgFLC, 10.4 times and 29 times, respectively; NOS2, 3.8 times and 4.5 times, respectively). After treatment, group D showed significantly decreased expression of IgFLC (5.0 times) and NOS2 (2.5 times). Conclusion The antiallergic effect of anti-IL-33 can be explained by suppression of IgFLC and NOS2 in a murine model of allergic rhinitis.
Background and Objectives: The immunomodulatory effects and mechanism of probiotics in allergic airway disease are largely unknown. We studied whether <i>Bacillus clausii</i> (BC), a probiotic derived from mudflats, had anti-allergic effects and compared the results with those of <i>Lactobacillus paracasei</i> (LP). We also examined whether the anti-allergic mechanisms of probiotics are associated with hypoxia signaling.Materials and Method: Forty-two BALB/c mice were randomly assigned to six experimental groups: controls, ovalbumin (OVA)-induced mice for inducing asthma, and OVA-induced mice that were orally administered LP or BC, at 1×10<sup>9</sup> or 5×10<sup>9</sup> CFU/mL each. We performed differential cell count testing on bronchoalveolar lavage fluid (BALF), lung histopathology, serum totals and OVA-specific IgE and IgG1 assessments, Th2 cytokine titers (IL-4, IL-5) in BALF and pulmonary parenchyma, quantitative PCR for <i>heme oxygenase (HO)-1</i> and <i>Hif-1α</i>, and immunohistochemistry.Results: Compared to the OVA group mice, OVA-sensitized mice treated with LP or BC showed significantly reduced numbers of eosinophils and neutrophils in the BALF (p<0.05). Both probiotics also significantly reduced pulmonary inflammation and eosinophil infiltration. Mice in the LP or BC group had a substantially lower titer of IL-4 and IL-5 in BALF, and decreased IL-4 and IL-5 expression in the lung parenchyma. Real-time PCR and immunohistochemistry showed that both LP and BC could significantly suppress <i>HO-1</i> and <i>Hif-1α</i> expression in asthmatic mice (p<0.05).Conclusion: BC can attenuate murine allergic asthma by regulating HIF-1α signaling, and its anti-allergic effect is comparable to that of LP.
BACKGROUND: Hind limb unloading (HU) is one of the ground-based models of simulated microgravity. As bacterial and viral infections could affect the immune system, the immunologic effect of HU should be studied in a specific-pathogen-free (SPF) laboratory. However, a review of the literature did not reveal any studies on the immunologic effects of prolonged HU in a murine model of allergic disease. Accordingly, the present study was undertaken to evaluate the effect of HU in a murine model of allergic asthma in a SPF laboratory. METHODS: Twenty BALB/c mice were allocated equally to Group A (control group), Group B (HU group), Group C (allergic group), or Group D (allergic + HU group). Weight gains, serum total and ovalbumin (OVA)-specific IgE, titers of IL-1, IL-5, IL-10, and IFN-γ in bronchoalveolar lavage (BAL) fluid, and histopathologic findings of the lungs were compared. RESULTS: After 2 wk of HU, Group D showed significantly more weight loss (−2.0 ± 0.2 g) than Group C (−1.1 ± 0.4 g). Groups B and D showed significant increases in serum OVA-specific IgE as compared with Groups A and C. Group D had significantly lower titers of IL-5 (Group C: 53.0 ± 15.2 pg · ml −1 , Group D: 21.9 ± 13.9 pg · ml −1 ), IL-10 (Group C: 430.8 ± 138.3 pg · ml −1 , Group D: 217.6 ± 51.2 pg · ml −1 ), and IFN-γ (Group C: 104.3 ± 37.5 pg · ml −1 , Group D: 36.7 ± 12.8 pg · ml −1 ) in BAL fluid than Group C. Peri-bronchiolar and pulmonary infiltrations of inflammatory cells were significantly greater in Group D than in Group C. CONCLUSIONS: Prolonged HU may cause significant weight loss and aggravate disease courses.Jang TY, Heo M-J, Jung A-Y, Kim YH. Prolonged anti-orthostatic hind limb unloading and murine allergic asthma . Aerosp Med Hum Perform. 2015; 86(9):803–807.
Abstract We aimed to evaluate the effect of chronic hypergravity in a mouse model of allergic asthma and rhinitis. Forty BALB/c mice were divided as: group A (n = 10, control) sensitized and challenged with saline, group B (n = 10, asthma) challenged by intraperitoneal and intranasal ovalbumin (OVA) to induce allergic asthma and rhinitis, and groups C (n = 10, asthma/rotatory control) and D (n = 10, asthma/hypergravity) exposed to 4 weeks of rotation with normogravity (1G) or hypergravity (5G) during induction of asthma/rhinitis. Group D showed significantly decreased eosinophils, neutrophils, and lymphocytes in their BAL fluid compared with groups B and C ( p < 0.05). In real-time polymerase chain reaction using lung homogenate, the expression of IL-1β was significantly upregulated ( p < 0.001) and IL-4 and IL-10 significantly downregulated ( p < 0.05) in group D. Infiltration of inflammatory cells into lung parenchyma and turbinate, and the thickness of respiratory epithelium was significantly reduced in group D ( p < 0.05). The expression of Bcl-2 and heme oxygenase-1 were significantly downregulated, Bax and extracellular dismutase significantly upregulated in Group D. Therefore, chronic hypergravity could have a hormetic effect for allergic asthma and rhinitis via regulation of genes involved in antioxidative and proapoptotic pathways. It is possible that we could use hypergravity machinery for treating allergic respiratory disorders.
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