Attenuation of Pulmonary Mycobacterium Avium Disease by Active Hexose Correlated Compound (AHCC) in MiceMasaki Fujita1*, Takemasa Matsumoto1, Ryosuke Hirano1, Kazunari Ishii2, Kenji Hiromatsu2, Junji Uchino1 and Kentaro Watanabe1
- *Corresponding Author:
- Masaki Fujita
Department of Respiratory Medicine, Faculty of Medicine
Fukuoka University, Fukuoka 814-0180, Japan
Tel: 81-92- 801-1011
E-mail: [email protected]
Received date: October 09, 2015; Accepted date: October 28, 2015; Published date: November 02, 2015
Citation: Fujita M, Matsumoto T, Hirano R, Ishii K, Hiromatsu K, et al. (2015) Attenuation of Pulmonary Mycobacterium Avium Disease by Active Hexose Correlated Compound (AHCC) in Mice. J Nutr Disorders Ther 5:174. doi:10.4172/2161-0509.1000174
Copyright: © 2015 Fujita M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Introduction: Pulmonary Mycobacterium avium disease is a chronic and progressive disease that is known to be difficult to treat. Active hexose correlated compound (AHCC) is an extract obtained by culturing mycelia of Basidiomycota. AHCC is reported to attenuate several experimental animal infection models. We hypothesized that AHCC could attenuate pulmonary M. avium disease in mice.
Methods: Mycobacterium avium (108 cfu/head) was administered intratracheally into mice (C57/BL6). Infected mice were supplied with 1,000 mg/kg/day of AHCC by oral administration until euthanasia. The mice were sacrificed at seven days later or 21 days later after M. avium infection. The lung homogenates were cultured on Middlebrook 7H10 agar plates for bacterial colony counts. Additionally, the number of inflammatory cells in the lungs was analyzed by FACS. Tissue sections of the lungs were stained by hematoxylin and eosin or Ziehl-Neelsen methods. In addition, the number of bacterial colonies in the
macrophages was counted in vitro. Approximately 1x106 macrophages were incubated with M. avium at an MOI of 10 with or without 1 mg/ml of AHCC.
Results: The administration of AHCC improved lung inflammation caused by M. avium according to the histology results and decreased number of M. avium in the lungs. In the analysis of lung inflammatory cells, the number of TNFR1 cells and NK cells remained unchanged by AHCC administration, however, the number of TNFR2 cells slightly increased. There was no difference in the number of M. avium in macrophages treated with or without AHCC in the in vitro study.
Conclusion: AHCC plays a protective role in a murine model of pulmonary M. avium disease.