| Title | Effect of amikacin on cell wall glycopeptidolipid synthesis in Mycobacterium abscessus |
|---|---|
| Author | So-Young Lee1, Hee-Youn Kim1, Byoung-Jun Kim1, Hong Kim1, Seung-hyeok Seok1, Bum-Joon Kim1,2,3, and Yoon-Hoh Kook1* |
| Address | 1Department of Microbiology and Immunology, Seoul National University Medical Research Center (SNUMRC), Seoul National University College of Medicine, Seoul 03080, Republic of Korea, 2Department of Biomedical Sciences, Seoul National University Medical Research Center (SNUMRC), Seoul National University College of Medicine, Seoul 03080, Republic of Korea, 3Cancer Research Institute, and Institute of Endemic Diseases, Seoul National University Medical Research Center (SNUMRC), Seoul National University College of Medicine, Seoul 03080, Republic of Korea |
| Bibliography | Journal of Microbiology, 55(8),640–647, 2017, |
| DOI | 10.1007/s12275-017-6503-7 |
| Key Words | Mycobacterium abscessus, glycopeptidolipid (GPL), amikacin, biofilm |
| Abstract | Cultivation of the smooth colony Mycobacterium abscessus at the sub-minimum inhibitory concentration (MIC) of amikacin changed its growth pattern including its colony morphology (smooth to rough) and cell arrangement (dispersed to cord formation). In addition, reduced sliding motility and biofilm formation were observed. The amount of glycogpetidolipid (GPL) and mRNA expression of key genes involved in GPL synthesis were decreased in the amikacin-treated M. abscessus strain. An in vitro infection assay revealed that the amikacin-treated smooth M. abscessus strain induced more pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) than that of the smooth strain in murine macrophage cells. These results suggest that long-term exposure to a low concentration of amikacin causes a physical change in the cell wall which may increase its virulence. |