Kyushu University Academic Staff Educational and Research Activities Database
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Mitsuteru Akahoshi Last modified date:2018.09.17



Graduate School
Undergraduate School
Other Organization
Administration Post
Other


E-Mail
Phone
092-642-5233
Fax
092-642-5247
Academic Degree
M.D., Ph.D
Field of Specialization
Rheumatology, Clinical Immunology
Research
Research Interests
  • The role of mast cells and their proteases in the pathogenesis of systemic sclerosis
    keyword : mast cell, systemic sclerosis, protease
    2016.04.
  • The role of mast cells in innate host defense against endogeneous and exogeneous toxic substances
    keyword : mast cell, venom, toxin, host defense
    2013.04.
Academic Activities
Reports
1. Miyake K, Akahoshi M, Nakashima H., Th subset balance in lupus nephritis., J Biomed Biotechnol., 2011.08, Lupus nephritis, which has various histological patterns and variable clinical outcomes, is one of the most important complications of systemic lupus nephritis (SLE). This pathogenetic mechanism in each histologically different type of lupus nephritis (LN) remains unclear. Although SLE is suggested to be a Th2-driven disease, elevation of both Th1 and Th2 cytokines occurs in both humans and mice, suggesting that SLE is a complex disease driven by different lymphocyte subsets with high heterogeneity of clinical manifestations and organ involvement. Recent findings in LN elucidate an essential role for the Th1, IL-17 producing T cells and Th17 cells in the development of diffuse proliferative lupus nephritis (DPLN), and Th2 cytokine in that of membranous lupus nephritis (MLN). These data support the hypothesis that individual Th1/Th2 balance is one of the critical determinants for histopathology of LN..
Papers
1. Akahoshi M, Song CH, Piliponsky AM, Metz M, Guzzetta A, Abrink M, Schlenner SM, Feyerabend TB, Rodewald HR, Pejler G, Tsai M, Galli SJ., Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice., J Clin Invest., 10.1172/JCI46139, 121, 10, 4180-4191, 2011.10, Mast cell degranulation is important in the pathogenesis of anaphylaxis and allergic disorders. Many animal venoms contain components that can induce mast cell degranulation, and this has been thought to contribute to the pathology and mortality caused by envenomation. However, we recently reported evidence that mast cells can enhance the resistance of mice to the venoms of certain snakes and that mouse mast cell-derived carboxypeptidase A3 (CPA3) can contribute to this effect. Here, we investigated whether mast cells can enhance resistance to the venom of the Gila monster, a toxic component of that venom (helodermin), and the structurally similar mammalian peptide, vasoactive intestinal polypeptide (VIP). Using 2 types of mast cell-deficient mice, as well as mice selectively lacking CPA3 activity or the chymase mouse mast cell protease-4 (MCPT4), we found that mast cells and MCPT4, which can degrade helodermin, can enhance host resistance to the toxicity of Gila monster venom. Mast cells and MCPT4 also can limit the toxicity associated with high concentrations of VIP and can reduce the morbidity and mortality induced by venoms from 2 species of scorpions. Our findings support the notion that mast cells can enhance innate defense by degradation of diverse animal toxins and that release of MCPT4, in addition to CPA3, can contribute to this mast cell function..
Membership in Academic Society
  • Japan Primary Care Association
Educational
Other Educational Activities
  • 2016.09.