Shunsuke Uno1, Tomoyasu Nishimura2, Kazumi Nishio3, Asami Kohsaka1, Eiko Tamizu1, Yasushi Nakano3, Junko Kagyo4, Yukiko Nakajima5, Ryosuke Arai3, Hanako Hasegawa3, Kenichi Arakawa6, Shoko Kashimura1, Ryota Ishii7, Naoki Miyazaki8, Yoshifumi Uwamino9, Naoki Hasegawa1. 1. Department of Infectious Diseases, Keio University School of Medicine, Japan. 2. Department of Infectious Diseases, Keio University School of Medicine, Japan; Keio University Health Center, Japan. Electronic address: tnishimura@keio.jp. 3. Department of Respiratory Medicine, Kawasaki Municipal Ida Hospital, Japan. 4. Department of Respiratory Medicine, Kawasaki Municipal Ida Hospital, Japan; Department of Respiratory Medicine, Keiyu Hospital, Japan. 5. Department of Infectious Diseases, Kawasaki Municipal Ida Hospital, Japan. 6. Department of Respiratory Medicine, Japan Anti-Tuberculosis Association Fukujuji Hospital, Japan. 7. Biostatistics Unit, Clinical and Translational Research Center, Keio University Hospital, Japan; Department of Biostatistics, Faculty of Medicine, University of Tsukuba, Japan. 8. Biostatistics Unit, Clinical and Translational Research Center, Keio University Hospital, Japan. 9. Department of Infectious Diseases, Keio University School of Medicine, Japan; Department of Laboratory Medicine, Keio University School of Medicine, Japan.
Abstract
OBJECTIVES: To determine the usefulness of hsa-miR-346, a potential biomarker enhancing the activity of non-tuberculous mycobacterial diseases, as a biomarker of tuberculosis activity. METHODS: We investigated whether hsa-miR-346 is secreted by human macrophages infected with Mycobacterium tuberculosis (M. tuberculosis) in an in vitro study. In addition, a cross-sectional study was conducted first to evaluate whether serum hsa-miR-346 is elevated in patients with tuberculosis compared with that in healthy individuals. Second, we conducted a retrospective study to evaluate whether anti-tuberculosis treatment reduces serum hsa-miR-346 levels. RESULTS: Log hsa-miR-346 levels were significantly elevated in the supernatant of human macrophages infected with M. tuberculosis in a dose-dependent manner. The mean serum log hsa-miR-346 levels were -15.48 (-15.76 to -15.21) in patients with tuberculosis and -16.12 (-16.29 to -15.95) in healthy volunteers, which significantly differed. In addition, hsa-miR-346 significantly decreased at 2 months from starting an anti-tuberculosis treatment. CONCLUSIONS: We consider hsa-miR-346 as a potential biomarker enhancing the tuberculosis activity.
OBJECTIVES: To determine the usefulness of hsa-miR-346, a potential biomarker enhancing the activity of non-tuberculous mycobacterial diseases, as a biomarker of tuberculosis activity. METHODS: We investigated whether hsa-miR-346 is secreted by human macrophages infected with Mycobacterium tuberculosis (M. tuberculosis) in an in vitro study. In addition, a cross-sectional study was conducted first to evaluate whether serum hsa-miR-346 is elevated in patients with tuberculosis compared with that in healthy individuals. Second, we conducted a retrospective study to evaluate whether anti-tuberculosis treatment reduces serum hsa-miR-346 levels. RESULTS: Log hsa-miR-346 levels were significantly elevated in the supernatant of human macrophages infected with M. tuberculosis in a dose-dependent manner. The mean serum log hsa-miR-346 levels were -15.48 (-15.76 to -15.21) in patients with tuberculosis and -16.12 (-16.29 to -15.95) in healthy volunteers, which significantly differed. In addition, hsa-miR-346 significantly decreased at 2 months from starting an anti-tuberculosis treatment. CONCLUSIONS: We consider hsa-miR-346 as a potential biomarker enhancing the tuberculosis activity.