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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


    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


    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


    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


    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 electron 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


    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


    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


    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


    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.