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Experimental Reactivation of Pulmonary Mycobacterium avium Complex Infection in a Modified Cornell-Like Murine Model

Authors
 Seung Bin Cha  ;  Bo Young Jeon  ;  Woo Sik Kim  ;  Jong-Seok Kim  ;  Hong Min Kim  ;  Kee Woong Kwon  ;  Sang-Nae Cho  ;  Sung Jae Shin  ;  Won-Jung Koh 
Citation
 PLOS ONE, Vol.10(9) : e0139251, 2015 
Journal Title
 PLOS ONE 
Issue Date
2015
MeSH
Animals ; Antitubercular Agents/pharmacology ; Bacterial Load ; Drug Resistance, Bacterial* ; Female ; Lung/microbiology* ; Mice ; Mice, Inbred C57BL ; Mycobacterium avium/drug effects ; Mycobacterium avium/pathogenicity* ; Mycobacterium avium Complex/drug effects ; Mycobacterium avium Complex/pathogenicity*
Abstract
The latency and reactivation of Mycobacterium tuberculosis infection has been well studied. However, there have been few studies of the latency and reactivation of Mycobacterium avium complex (MAC), the most common etiological non-tuberculous Mycobacterium species next to M. tuberculosis in humans worldwide. We hypothesized that latent MAC infections can be reactivated following immunosuppression after combination chemotherapy with clarithromycin and rifampicin under experimental conditions. To this end, we employed a modified Cornell-like murine model of tuberculosis and investigated six strains consisting of two type strains and four clinical isolates of M. avium and M. intracellulare. After aerosol infection of each MAC strain, five to six mice per group were euthanized at 2, 4, 10, 18, 28 and 35 weeks post-infection, and lungs were sampled to analyze bacterial burden and histopathology. One strain of each species maintained a culture-negative state for 10 weeks after completion of 6 weeks of chemotherapy, but was reactivated after 5 weeks of immunosuppression in the lungs with dexamethasone (three out of six mice in M. avium infection) or sulfasalazine (four out of six mice in both M. avium and M. intracellulare infection). The four remaining MAC strains exhibited decreased bacterial loads in response to chemotherapy; however, they remained at detectable levels and underwent regrowth after immunosuppression. In addition, the exacerbated lung pathology demonstrated a correlation with bacterial burden after reactivation. In conclusion, our results suggest the possibility of MAC reactivation in an experimental mouse model, and experimentally demonstrate that a compromised immune status can induce reactivation and/or regrowth of MAC infection.
Files in This Item:
T201503776.pdf Download
DOI
10.1371/journal.pone.0139251
Appears in Collections:
5. Research Institutes (연구소) > Institute for Immunology and Immunological Disease (면역질환연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Kim, Jong Seok(김종석)
Shin, Sung Jae(신성재) ORCID logo https://orcid.org/0000-0003-0854-4582
Cho, Sang Nae(조상래)
Cha, Seung Bin(차승빈)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/141306
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