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Allergic Inflammation

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Kazuo Ohuchi – One of the best experts on this subject based on the ideXlab platform.

  • Analysis of the Leukotriene D4 Receptor in the Granulation Tissue of Allergic Inflammation in Rats
    International Archives of Allergy and Immunology, 2009
    Co-Authors: Noriyasu Hirasawa, Tomonori Hoshi, Michiko Kudoh, Suetsugu Mue, Susumu Tsurufuji, Masako Watanabe, Kazuo Ohuchi
    Abstract:

    Leukotriene (LT) D4 receptor in the granulation tissue formed in the air pouch-type Allergic Inflammation model in rats was analyzed. Membrane preparation of the granulation tissue obtained

  • Possible participation of cyclooxygenase-2 in the recurrence of Allergic Inflammation in rats.
    European Journal of Pharmacology, 1997
    Co-Authors: Hisae Niki, Suetsugu Mue, Yuhji Tominaga, Masako Watanabe-kobayashi, Kazuo Ohuchi
    Abstract:

    In the recurrence of Allergic Inflammation in a rat air pouch model, pouch fluid volume, prostaglandin E2 concentration in the pouch fluid, leukocyte infiltration into the pouch fluid, and granulation tissue weight were markedly increased by the antigen challenge. To clarify the role of cyclooxygenase-2 in the recurrence of Allergic Inflammation, the time-course of changes in protein levels of cyclooxygenase-1 and cyclooxygenase-2 in the granulation tissue and in the infiltrated leukocytes was examined by Western blot analysis. It was shown that cyclooxygenase-1 levels in the granulation tissue and in the infiltrated leukocytes were not changed by the antigen challenge, but cyclooxygenase-2 levels were increased. Furthermore, treatment with the selective cyclooxygenase-2 inhibitor, NS-398 ([N-2(cyclohexyloxy-4-nitrophenyl]-methanesulfonamide), suppressed the recurrence of Allergic Inflammation as did the non-selective cyclooxygenase-1/cyclooxygenase-2 inhibitor, indomethacin. The steroidal anti-inflammatory drug, dexamethasone, inhibited the induction of cyclooxygenase-2, and suppressed the Allergic Inflammation. These findings strongly suggested that cyclooxygenase-2 induced by the antigen challenge plays a role in the recurrence of Inflammation induced by the Allergic mechanism.

  • The mechanism of histamine production in Allergic Inflammation.
    Methods and Findings in Experimental and Clinical Pharmacology, 1995
    Co-Authors: Noriyasu Hirasawa, Kazuo Ohuchi
    Abstract:

    In the air pouch-type Allergic Inflammation model in rats, histamine produced in the late phase plays a role in downregulation of leukocyte infiltration into the pouch fluid. In the pouch fluid, we found two kinds of histamine production-increasing factor (HPIF) ; HPIF-1, which induces histamine production in bone marrow cells, and HPIF-2, which enhances the activity of HPIF-1. Isoelectric point and molecular weight of HPIF-1 and HPIF-2 were estimated to be pI 4-5 and 25-40 kD, and pI 7-8 and about 100 kD, respectively. The histamine-producing ability of bone marrow cells increased after the antigen challenge, but that of peripheral leukocytes decreased markedly 8 h after the antigen challenge. Pharmacological analysis indicated that HPIF-1 induces histamine production through activation of protein kinase C and tyrosine kinase. Differentiation of bone marrow cells to histamine-producing cells by HPIF-1 was also indicated. From these observations the histamine production in the late phase of Allergic Inflammation is suggested to be regulated by the production of HPIF-1, proliferation/differentiation of histamine-producing cells, and infiltration of histamine-producing cells in blood circulation into the inflammatory site.

Dooil Jeoung – One of the best experts on this subject based on the ideXlab platform.

  • mir 135 5p p62 axis regulates autophagic flux tumorigenic potential and cellular interactions mediated by extracellular vesicles during Allergic Inflammation
    Frontiers in Immunology, 2019
    Co-Authors: Yeongseo Park, Jaehwan Byun, Yoojung Kwon, Myeong Seon Jeong, Hyun Suk Jung, Dooil Jeoung
    Abstract:

    The objective of this study was to investigate the relationship between autophagy and Allergic Inflammation. In vitro Allergic Inflammation was accompanied by an increased autophagic flux in rat basophilic leukemia (RBL2H3) cells. 3-MA, an inhibitor of autophagic processes, negatively regulated Allergic Inflammation both in vitro and in vivo. The role of p62, a selective receptor of autophagy, in Allergic Inflammation was investigated. P62, increased by antigen stimulation, mediated in vitro Allergic Inflammation, passive cutaneous anaphylaxis (PCA), and passive systemic anaphylaxis (PSA). P62 mediated cellular interactions during Allergic Inflammation. It also mediated tumorigenic and metastatic potential of cancer cells enhanced by PSA. TargetScan analysis predicted that miR-135-5p was a negative regulator of p62. Luciferase activity assay showed that miR-135-5p directly regulated p62. MiR-135-5p mimic negatively regulated features of Allergic Inflammation and inhibited tumorigenic and metastatic potential of cancer cells enhanced by PSA. MiR-135-5p mimic also inhibited cellular interactions during Allergic Inflammation. Extracellular vesicles mediated Allergic Inflammation both in vitro and in vivo. Extracellular vesicles were also necessary for cellular interactions during Allergic Inflammation. Transmission elecelectron microscopy showed p62 within extracellular vesicles of antigen-stimulated rat basophilic leukemia cells (RBL2H3). Extracellular vesicles isolated from antigen-stimulated RBL2H3 cells induced activation of macrophages and enhanced invasion and migration potential of B16F1 mouse melanoma cells in a p62-dependent manner. Extracellular vesicles isolated from PSA-activated BALB/C mouse enhanced invasion and migration potential of B16F1 cells, and induced features of Allergic Inflammation in RBL2H3 cells. Thus, miR-135-5p-p62 axis might serve as a target for developing anti-allergy drugs.

  • The Hyaluronic Acid-HDAC3-miRNA Network in Allergic Inflammation.
    Frontiers in immunology, 2015
    Co-Authors: Youngmi Kim, Hyuna Kim, Sangkyung Eom, Deokbum Park, Dooil Jeoung
    Abstract:

    We previously reported the anti-Allergic effect of high molecular weight form of hyaluronic acid (HMW-HA). In doing so, HA targets CD44 and inhibits FceRI signaling and cross-talk between epidermal growth factor receptor (EGFR) and FceRI. We previously reported the role of histone deacetylases (HDACs) in Allergic Inflammation and Allergic Inflammation-promoted enhanced tumorigenic potential. We reported regulatory role of HA in the expression of HDAC3. In this review, we will discuss molecular mechanisms associated with anti-Allergic effect of hyaluronic acid in relation with HDACs. The role of microRNAs (miRNAs) in Allergic Inflammation has been reported. We will also discuss the role of miRNAs in Allergic Inflammation in relation with HA-mediated anti-Allergic effects.

  • Transglutaminase II/MicroRNA-218/-181a Loop Regulates Positive Feedback Relationship between Allergic Inflammation and Tumor Metastasis
    The Journal of biological chemistry, 2014
    Co-Authors: Sangkyung Eom, Jongseon Choe, Misun Kim, Youngmi Kim, Hansoo Lee, Yun-sil Lee, Deokbum Park, Young Myeong Kim, Dooil Jeoung
    Abstract:

    The molecular mechanism of transglutaminase II (TGaseII)-mediated Allergic Inflammation remains largely unknown. TGaseII, induced by antigen stimulation, showed an interaction and co-localization with FcϵRI. TGaseII was necessary for in vivo Allergic Inflammation, such as triphasic cutaneous reaction, passive cutaneous anaphylaxis, and passive systemic anaphylaxis. TGaseII was necessary for the enhanced metastatic potential of B16F1 melanoma cells by passive systemic anaphylaxis. TGaseII was shown to be a secreted protein. Recombinant TGaseII protein increased the histamine release and β-hexosaminidase activity, and enhanced the metastatic potential of B16F1 mouse melanoma cells. Recombinant TGaseII protein induced the activation of EGF receptor and an interaction between EGF receptor and FcϵRI. Recombinant TGaseII protein displayed angiogenic potential accompanied by Allergic Inflammation. R2 peptide, an inhibitor of TGaseII, exerted negative effects on in vitro and in vivo Allergic Inflammation by regulating the expression of TGaseII and FcϵRI signaling. MicroRNA (miR)-218 and miR-181a, decreased during Allergic Inflammation, were predicted as negative regulators of TGaseII by microRNA array and TargetScan analysis. miR-218 and miR-181a formed a negative feedback loop with TGaseII and regulated the in vitro and in vivo Allergic Inflammation. TGaseII was necessary for the interaction between mast cells and macrophages during Allergic Inflammation. Mast cells and macrophages, activated during Allergic Inflammation, were responsible for the enhanced metastatic potential of tumor cells that are accompanied by Allergic Inflammation. In conclusion, the TGaseII/miR-218/-181a feedback loop can be employed for the development of anti-allergy therapeutics.

Yong-jun Liu – One of the best experts on this subject based on the ideXlab platform.

  • The IL-17 cytokine family and their role in Allergic Inflammation.
    Current opinion in immunology, 2008
    Co-Authors: Yui-hsi Wang, Yong-jun Liu
    Abstract:

    Allergic diseases and asthma has long been hypothesized as the results of the dysregulation of type 2 immune responses to environmental allergens. Recent progresses in characterizing the proinflammatory IL-17 cytokine family have added additional layer of complexity on the regulation of Allergic Inflammation. The delineation of IL-17-producing CD4+ T cell subset (Th17) has led to the revision of Th1/Th2 paradigm and impacts our perspectives on the basis of chronic tissue Inflammation. In addition, the distinctive expression patterns and biological activities of individual IL-17 cytokine member may play different roles in the regulation of the pathogenesis of Allergic diseases. Understanding the cellular source and targeting cells of IL-17 cytokine family member will provide the basis to elucidate the cellular mechanism underlying Allergic Inflammation and improve our therapeutic approaches for allergy.

  • Thymic stromal lymphopoietin: master switch for Allergic Inflammation
    The Journal of experimental medicine, 2006
    Co-Authors: Yong-jun Liu
    Abstract:

    Thymic stromal lymphopoietin (TSLP) is an interleukin (IL) 7–like cytokine that triggers dendritic cell–mediated T helper (Th)2 inflammatory responses. TSLP is highly expressed by keratinocytes in skin lesions of patients with atopic dermatitis and is associated with dendritic cell activation in situ, suggesting that TSLP might be a master switch for Allergic Inflammation at the epithelial cell–dendritic cell interface. New reports now establish a direct link between TSLP expression and the pathogenesis of atopic dermatitis and asthma in vivo, and begin to reveal the molecular mechanisms underlying TSLP-induced Allergic Inflammation.

Jongseon Choe – One of the best experts on this subject based on the ideXlab platform.

  • miR-122-SOCS1-JAK2 axis regulates Allergic Inflammation and Allergic Inflammation-promoted cellular interactions.
    Oncotarget, 2017
    Co-Authors: Kyeonga Noh, Misun Kim, Youngmi Kim, Hanearl Kim, Hyuna Kim, Jaehwan Byun, Yeongseo Park, Hansoo Lee, Yun-sil Lee, Jongseon Choe
    Abstract:

    // Kyeonga Noh 1, * , Misun Kim 1, * , Youngmi Kim 1, * , Hanearl Kim 1 , Hyuna Kim 1 , Jaehwan Byun 1 , Yeongseo Park 1 , Hansoo Lee 2 , Yun Sil Lee 3 , Jongseon Choe 4 , Young Myeong Kim 4 and Dooil Jeoung 1 1 Department of Biochemistry, Kangwon National University, Chunchon 24341, Korea 2 Department of Biological Sciences, Kangwon National University, Chunchon 24341, Korea 3 College of Pharmacy, Ewha Womans University, Seoul 03760, Korea 4 Graduate School of Medicine, Kangwon National University, Chunchon 24341, Korea * These authors have contributed equally to this work Correspondence to: Dooil Jeoung, email: jeoungd@kangwon.ac.kr Keywords: Allergic Inflammation, cellular interaction, miR-122, SOCS1, tumor microenvironments Received: December 09, 2016     Accepted: June 19, 2017     Published: July 10, 2017 ABSTRACT The regulatory role of suppressor of cytokine signaling 1 (SOCS1) in Inflammation has been reported. However, its role in Allergic Inflammation has not been previously reported. SOCS1 mediated in vitro and in vivo Allergic Inflammation. Histone deacetylase-3 (HDAC3), a mediator of Allergic Inflammation, interacted with SOCS1, and miR-384 inhibitor, a positive regulator of HDAC3, induced features of Allergic Inflammation in an SOCS1-dependent manner. miRNA array analysis showed that the expression of miR-122 was decreased by antigenstimulation. TargetScan analysis predicted the binding of miR-122 to the 3′-UTR of SOCS1. miR-122 inhibitor induced in vitro and in vivo Allergic features in SOCS1-dependent manner. SOCS1 was necessary for Allergic Inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells. SOCS1 and miR-122 regulated cellular interactions involving cancer cells, mast cells and macrophages during Allergic Inflammation. SOCS1 mimetic peptide, D-T-H-F-R-T-F-R-S-H-S-D-Y-R-R-I, inhibited in vitro and in vivo Allergic Inflammation, Allergic Inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells, and cellular interactions during Allergic Inflammation. Janus kinase 2 (JAK2) exhibited binding to SOCS1 mimetic peptide and mediated Allergic Inflammation. Transforming growth factor– s1 (TGF-s1) was decreased during Allergic Inflammation and showed an anti-Allergic effect. SOCS1 and JAK2 regulated the production of anti-Allergic TGF-s1. Taken together, our results show that miR-122-SOCS1 feedback loop can be employed as a target for the development of anti-Allergic and anti-cancer drugs.

  • MicroRNA-26a/-26b-COX-2-MIP-2 Loop Regulates Allergic Inflammation and Allergic Inflammation-promoted Enhanced Tumorigenic and Metastatic Potential of Cancer Cells
    The Journal of biological chemistry, 2015
    Co-Authors: Yoojung Kwon, Kyeonga Noh, Misun Kim, Youngmi Kim, Hyuna Kim, Hansoo Lee, Yun-sil Lee, Sangkyung Eom, Deokbum Park, Jongseon Choe
    Abstract:

    Abstract Cyclooxgenase-2 (COX-2) knockout mice experiments showed that COX-2 was necessary for in vivo Allergic Inflammation such as passive cutaneous anaphylaxis (PCA), passive systemic anaphylaxis (PSA) and triphasic cutaneous Allergic reaction (TpCR). TargetScan analysis predicted COX-2 as a target of miR-26a and miR-26b. miR-26a/-26b decreased luciferase activity associated with COX-2-3′UTR. miR-26a/-26b exerted negative effects on the features of in vitro and in vivo Allergic Inflammation by targeting COX-2. ChIP assays showed the binding of HDAC3 and SNAIL, but not COX-2, to the promoter sequences of miR-26a and miR-26b. Cytokine array analysis showed that the induction of chemokines, such as MIP-2, in the mouse PSA model occurred in a COX-2 dependent manner. ChIP assays showed the binding of HDAC3 and COX-2 to the promoter sequences of MIP-2. In vitro and in vivo Allergic Inflammation was accompanied by the increased expression of MIP-2. miR-26a/-26b negatively regulated the expression of MIP-2. Allergic Inflammation enhanced the tumorigenic and metastatic potential of cancer cells and induced positive feedback involving cancer cells and stromal cells such as mast cells, macrophages and endothelial cells. miR-26a mimic and miR-26b mimic negatively regulated the positive feedback between cancer cells and stromal cells and the positive feedback among stromal cells. miR-26a/-26b negatively regulated the enhanced tumorigenic potential by Allergic Inflammation. COX-2 was necessary for the enhanced metastatic potential of cancer cells by Allergic Inflammation. Taken together, our results indicate that miR26a/-26b-COX-2-MIP-2 loop regulates Allergic Inflammation and feedback relationship between Allergic Inflammation and the enhanced tumorigenic and metastatic potential.

  • Transglutaminase II/MicroRNA-218/-181a Loop Regulates Positive Feedback Relationship between Allergic Inflammation and Tumor Metastasis
    The Journal of biological chemistry, 2014
    Co-Authors: Sangkyung Eom, Jongseon Choe, Misun Kim, Youngmi Kim, Hansoo Lee, Yun-sil Lee, Deokbum Park, Young Myeong Kim, Dooil Jeoung
    Abstract:

    The molecular mechanism of transglutaminase II (TGaseII)-mediated Allergic Inflammation remains largely unknown. TGaseII, induced by antigen stimulation, showed an interaction and co-localization with FcϵRI. TGaseII was necessary for in vivo Allergic Inflammation, such as triphasic cutaneous reaction, passive cutaneous anaphylaxis, and passive systemic anaphylaxis. TGaseII was necessary for the enhanced metastatic potential of B16F1 melanoma cells by passive systemic anaphylaxis. TGaseII was shown to be a secreted protein. Recombinant TGaseII protein increased the histamine release and β-hexosaminidase activity, and enhanced the metastatic potential of B16F1 mouse melanoma cells. Recombinant TGaseII protein induced the activation of EGF receptor and an interaction between EGF receptor and FcϵRI. Recombinant TGaseII protein displayed angiogenic potential accompanied by Allergic Inflammation. R2 peptide, an inhibitor of TGaseII, exerted negative effects on in vitro and in vivo Allergic Inflammation by regulating the expression of TGaseII and FcϵRI signaling. MicroRNA (miR)-218 and miR-181a, decreased during Allergic Inflammation, were predicted as negative regulators of TGaseII by microRNA array and TargetScan analysis. miR-218 and miR-181a formed a negative feedback loop with TGaseII and regulated the in vitro and in vivo Allergic Inflammation. TGaseII was necessary for the interaction between mast cells and macrophages during Allergic Inflammation. Mast cells and macrophages, activated during Allergic Inflammation, were responsible for the enhanced metastatic potential of tumor cells that are accompanied by Allergic Inflammation. In conclusion, the TGaseII/miR-218/-181a feedback loop can be employed for the development of anti-allergy therapeutics.

Mark H. Kaplan – One of the best experts on this subject based on the ideXlab platform.

  • TH9 cells are required for tissue mast cell accumulation during Allergic Inflammation
    The Journal of allergy and clinical immunology, 2015
    Co-Authors: Sarita Sehra, Weiguo Yao, Evelyn T. Nguyen, Nicole L. Glosson-byers, Nahid Akhtar, Baohua Zhou, Mark H. Kaplan
    Abstract:

    Background IL-9 is important for the growth and survival of mast cells. IL-9 is produced by T cells, natural killer T cells, mast cells, eosinophils, and innate lymphoid cells, although the cells required for mast cell accumulation during Allergic Inflammation remain undefined. Objective We sought to elucidate the role of T H 9 cells in promoting mast cell accumulation in models of Allergic lung Inflammation. Methods Adoptive transfer of ovalbumin-specific T H 2 and T H 9 cells was used to assess the ability of each subset to mediate mast cell accumulation in tissues. Mast cell accumulation was assessed in wild-type mice and mice with PU.1-deficient T cells subjected to acute and chronic models of Allergic Inflammation. Results Adoptive transfer experiments demonstrated that recipients of T H 9 cells had significantly higher mast cell accumulation and expression of mast cell proteases compared with control or T H 2 recipients. Mast cell accumulation was dependent on IL-9, but not IL-13, a cytokine required for many aspects of Allergic Inflammation. In models of acute and chronic Allergic Inflammation, decreased IL-9 levels in mice with PU.1-deficient T cells corresponded to diminished tissue mast cell numbers and expression of mast cell proteases. Mice with PU.1-deficient T cells have defects in IL-9 production from CD4 + T cells, but not natural killer T cells or innate lymphoid cells, suggesting a T H cell–dependent phenotype. Rag1 −/− mice subjected to a chronic model of Allergic Inflammation displayed reduced mast cell infiltration comparable with accumulation in mice with PU.1-deficient T cells, emphasizing the importance of IL-9 produced by T cells in mast cell recruitment. Conclusion T H 9 cells are a major source of IL-9 in models of Allergic Inflammation and play an important role in mast cell accumulation and activation.

  • Wheezing and itching: The requirement for STAT proteins in Allergic Inflammation
    JAK-STAT, 2012
    Co-Authors: Nicole L. Glosson, Heather A. Bruns, Mark H. Kaplan
    Abstract:

    The development of Allergic Inflammation requires the orchestration of gene expression from the inflamed tissue and from the infiltrating immune cells. Since many of the cytokines that promote Allergic Inflammation signal through hematopoietin family receptors, the Signal Transducer and Activator of Transcription (STAT) family have obligate roles in pro-Allergic cytokine-induced gene regulation in multiple cell types. In this review, we summarize work defining the contribution of each of the STAT family members to the development of Allergic Inflammation, using data from mouse models of Allergic Inflammation, studies on patient samples and correlations with single nucleotide polymorphisms in STAT genes.