• Title, Summary, Keyword: Allergic inflammation

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TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice

  • Kim, Tae-Hyoun;Kim, Dong-Jae;Park, Jae-Hak;Park, Jong-Hwan
    • IMMUNE NETWORK
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    • v.14 no.5
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    • pp.249-254
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    • 2014
  • Allergic asthma is a chronic pulmonary inflammatory disease characterized by reversible airway obstruction, hyperresponsiveness and eosinophils infiltration. Toll-like receptors (TLRs) signaling are closely associated with asthma and have emerged as a novel therapeutic target in allergic disease. The functions of TLR3 and TLR4 in allergic airway inflammation have been studied; however, the precise role of TIR-domain-containing adapter-inducing interferon-${\beta}$ (TRIF), the adaptor molecule for both TLR3 and TLR4, is not yet fully understood. To investigate this, we developed a mouse model of OVA-induced allergic airway inflammation and compared the severity of allergic airway inflammation in WT and $TRIF^-/^-$ mice. Histopathological assessment revealed that the severity of inflammation in airway inflammation in TRIF-deficient mice was comparable to that in WT mice. The total number of cells recovered from bronchoalveolar lavage fluid did not differ between WT and TRIF-deficient mice. Moreover, TRIF deficiency did not affect Th1 and Th2 cytokine production in lung tissue nor the level of serum OVA-specific IgE, $IgG_1$ and $IgG_{2c}$. These findings suggest that TRIF-mediated signaling may not be critical for the development of allergic airway inflammation.

Effects of Ascaris suum Extract and Sulfamethoxazole on Allergic Airway Inflammation

  • Cho, Eun-Sang;Park, Bae-Keun;Son, Hwa-Young
    • Biomolecules & Therapeutics
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    • v.19 no.4
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    • pp.466-471
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    • 2011
  • Allergic asthma is complex inflammatory airway disorder caused by genetic and environmental factors. Sulfamethoxazole, a sulfonamide, is the cause of drug rash with eosinophilia and systemic symptoms syndrome. Parasites infection also related with eosinophilia and allergic diseases. In the present study, we investigated the modulating effects of parasitic derivative and sulfamethoxazole (SMX) on allergic airway inflammation in the ovalbumin (OVA)-induced murine asthma model. Histopathological changes, cytokine secretion, and total and allergen-specific IgE were investigated. BALB/c mice were treated with Ascaris suum extract or SMX for 4 weeks before sensitized and challenged to ovalbumin. Pre-treatment of Ascaris suum extract decreased allergic inflammation in lung tissue and IL-4, total IgE, and OVA-specific IgE levels in bronchoalveolar lavage fluid. However, pre-treatment of SMX did not show any effects on allergic airway inflammation. These results indicate that parasitic infection has protective effects on allergic asthma, but the sulfamamides may not relate with allergic asthma.

Analysis of chemical mediators and cytokines in allergic inflammation models in rats and their advantages for the screening of anti-allergic inflammatory drugs

  • Ohuchi, Kazuo
    • Proceedings of the Korean Society of Applied Pharmacology
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    • pp.11-18
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    • 1996
  • We have established an air pouch-type allergic inflammation model in rats [1,2] and a peritoneal eosinophilia model in rats [3]. Employing the two models, chemical mediators and cytokines responsible for the development of inflammation induced by at allergic mechanisms are investigated to clarify the usefulness of the two models for the screening of anti-allergic inflammatory drugs.

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Adenophorae Radix Attenuates Mast Cell-mediated Allergic Inflammation through Down-regulation of NF-κB/ Caspase-1 Activation

  • Myung, Noh-Yil
    • Korean Journal of Plant Resources
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    • v.33 no.6
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    • pp.659-665
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    • 2020
  • Adenophorae Radix (AR) has been used as a traditional medicine for various diseases. However, the regulatory mechanisms of AR in allergic inflammation are not yet understood. The present study was conducted to investigate the effect and mechanisms of AR on the mast cell-mediated allergic response. To determine the pharmacological mechanisms of AR in allergic inflammation, we evaluated the effects of AR on the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-8 as well as the activation of nuclear factor-κB (NF-κB) and caspase-1 in phorbol 12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-stimulated human mast cells (HMC-1). Our results demonstrated that AR effectively attenuated the PMACI-induced production of TNF-α, IL-6, IL-1β and IL-8 in stimulated HMC-1. Additionally, we showed that the inhibitory effect of AR on inflammatory cytokines in PMACI-stimulated HMC-1 cells involved the suppression of the activation NF-kB/caspase-1 in PMACI-stimulated HMC-1. Collectively, these findings provide experimental evidence that AR may be a useful candidate for the treatment of allergic inflammation.

Anti-allergic effects of So-Cheong-Ryong-Tang in ovalbumin-induced allergic rhinitis model (난알부민 유도 알레르기 비염 마우스에 대한 소청룡탕(小靑龍湯)의 효능 실험연구)

  • Kim, Ilhwan;Ku, Jinmo;Hur, Hansol;Na, Changhyeok;Jang, Bo-Hyoung;Shin, Yong-Cheol;Ko, Seong-Gyu
    • Journal of Society of Preventive Korean Medicine
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    • v.18 no.3
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    • pp.69-80
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    • 2014
  • Objective : Allergic rhinitis (AR) is an allergic inflammation of the nasal airways. Socheongryong-Tang traditionally has been used in Korea for treatment of allergy diseases. In the present study, we investigated whether SCRT suppresses the progression of AR in vivo and in vitro. Method : In this study, we investigated the effect of oral administration of SCRT on the Ovalbumin(OVA)-induced allergic rhinitis mouse models. Additionally, to find a possible explanation for the anti-inflammation effects of SCRT, we evaluated the inflammatory cytokine levels in LPS-stimulated mouse inflammation cell (RAW264.7) and mouse splenocyte. Results : The finding of this study demonstrated that SCRT reduced mast cells and inflammation cells infiltration in OVA-induced nasal cavity. Additionally, SCRT inhibited the production of inflammatory cytokines in splenocyte. However SCRT don't inhibited the production of inflammatory cytokines in RAW264.7 cells. Conclusion : Taken together, our results showed that oral administration of SCRT beneficial effects in allergic rhinitis, suggesting that SCRT might be a useful candidate for the treatment of allergic rhinitis.

Suppressive Effects of Benincasae hispida on Allergic Inflammation

  • Park, Seul-Ki;Kim, Jum-Ji;Sung, Sang-Min;Lee, Mi-Young
    • Molecular & Cellular Toxicology
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    • v.5 no.4
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    • pp.304-309
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    • 2009
  • The effects of an extract of Benincasae hispida on allergic inflammation were examined in terms of histamine and $\beta$-hexosaminidase release, serum IgE level and inflammatory cytokine level. The B. hispida extract inhibited the release of histamine and $\beta$-hexosaminidase, a degranulation marker, from rat basophilic leukemia cells (RBL-2H3). When mice were first ovalbumin-challenged and then treated with B. hispida extract, there was a significant decrease in the IgE level in the mouse serum. The extract treatment reduced the serum IgE level prominently, compared with the ovalbumin-challenged mice. The extract also significantly reduced the TNF-$\alpha$ and IL-4 levels in the BAL fluid when challenged with antigen. Taken together, the Benincasae hispida extract may be efficacious against allergic inflammation.

Inhibitory Effects of Water Extract of Lindera obtusiloba on the Mast Cell-Mediated Allergic Inflammation (생강나무 추출물의 알레르기성 염증반응 억제 효과)

  • Kim, Sang-Hyun;Son, Jun-Ho;Lee, Seung-Ho
    • Korean Journal of Pharmacognosy
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    • v.40 no.3
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    • pp.233-237
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    • 2009
  • Lindera obtusiloba has been used for centuries as a traditional medicine in Korea and recently known to have an anti-fibrotic effect. In this report, we investigated the effect of hot water extract from L. obtusiloba (WELB) on the mast cell-mediated allergic inflammation and studied its possible mechanisms of action. WELB inhibited phorbol-12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-induced histamine release in HMC-1 human mast cells. WELB reduced PMACI-induced gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor-$\alpha$, interleukin (IL)-$1{\beta}$, IL-6, and IL-8. The inhibitory effect of WELB on the expression of proinflammatory cytokines was c-jun N-terminal kinase and nuclear factor-${\kappa}B$ dependent. These results indicate that WELB may be beneficial in the treatment of mast cell-mediated allergic inflammation.

Inhibitory Effect of Ore Minerals on the Allergic Inflammation in Mouse

  • Park, Seul-Ki;Lee, Chang-Won;Lee, Mi-Young
    • Applied Biological Chemistry
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    • v.51 no.4
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    • pp.269-275
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    • 2008
  • The ore minerals, mainly composed of sericite, talc, and halloysite, were investigated for their inhibitory effect on the allergic inflammation in mice by measuring the serum IgE level, inflammatory cytokine production, and histamine and ${\beta}$-hexosaminidase releases. When the mice were ovalbumin (OVA)-challenged prior to the ore mineral treatment, the IgE level in the serum decreased significantly. The ore minerals significantly reduced the productions of IL-4 and the tumor necrosis factor-${\alpha}$ in the bronchial alveolar lavage fluid challenged with OVA. The inflammatory infiltrates, found in the lung of the OVA-challenged mouse, were also notably decreased following the ore mineral treatment. The ore minerals significantly reduced the release of histamine and ${\beta}$-hexosaminidase from the RBL-2H3 cells. These results suggest that the ore minerals may be useful as potent inhibitors of the allergic inflammation in mice.

Suppressive Effect of 4-Hydroxy-2-(4-Hydroxyphenethyl) Isoindoline-1,3-Dione on Ovalbumin-Induced Allergic Asthma

  • Huang, Jin;Su, Mingzhi;Lee, Bo-Kyung;Kim, Mee-Jeong;Jung, Jee H.;Im, Dong-Soon
    • Biomolecules & Therapeutics
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    • v.26 no.6
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    • pp.539-545
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    • 2018
  • 4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound. PD1 has peroxisome proliferator-activated receptor (PPAR) ${\gamma}$ agonistic and anti-inflammatory effects. This study aimed to investigate the effect of PD1 on allergic asthma using rat basophilic leukemia (RBL)-2H3 mast cells and an ovalbumin (OVA)-induced asthma mouse model. In vitro, PD1 suppressed ${\beta}$-hexosaminidase activity in RBL-2H3 cells. In the OVA-induced allergic asthma mouse model, increased inflammatory cells and elevated Th2 and Th1 cytokine levels were observed in bronchoalveolar lavage fluid (BALF) and lung tissue. PD1 administration decreased the numbers of inflammatory cells, especially eosinophils, and reduced the mRNA and protein levels of the Th2 cytokines including interleukin (IL)-4 and IL-13, in BALF and lung tissue. The severity of inflammation and mucin secretion in the lungs of PD1-treated mice was also less. These findings indicate that PD1 could be a potential compound for anti-allergic therapy.

Ginsenoside Rg3 suppresses mast cell-mediated allergic inflammation via mitogen-activated protein kinase signaling pathway

  • Kee, Ji-Ye;Hong, Seung-Heon
    • Journal of Ginseng Research
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    • v.43 no.2
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    • pp.282-290
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    • 2019
  • Background: Ginsenoside Rg3 (G-Rg3) is the major bioactive ingredient of Panax ginseng and has many pharmacological effects, including antiadipogenic, antiviral, and anticancer effects. However, the effect of G-Rg3 on mast cell-mediated allergic inflammation has not been investigated. Method: The antiallergic effects of G-Rg3 on allergic inflammation were evaluated using the human and rat mast cell lines HMC-1 and RBL-2H3. Antiallergic effects of G-Rg3 were detected by measuring cyclic adenosine monophosphate (cAMP), detecting calcium influx, and using real-time reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, Western blotting, and in vivo experiments. Results: G-Rg3 decreased histamine release from activated mast cells by enhancing cAMP levels and calcium influx. Proinflammatory cytokine production was suppressed by G-Rg3 treatment via regulation of the mitogen-activated protein kinases/nuclear factor-kappa B and receptor-interacting protein kinase 2 (RIP2)/caspase-1 signaling pathway in mast cells. Moreover, G-Rg3 protected mice against the IgE-mediated passive cutaneous anaphylaxis reaction and compound 48/80-induced anaphylactic shock. Conclusion: G-Rg3 may serve as an alternative therapeutic agent for improving allergic inflammatory disorders.