N-acetyl-cysteine mediates protection against Mycobacterium avium through induction of human β-defensin-2 in a mouse lung infection model
Microbes and Infection, ISSN: 1286-4579, Vol: 22, Issue: 10, Page: 567-575
2020
- 11Citations
- 11Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations11
- Citation Indexes11
- CrossRef11
- 11
- Captures11
- Readers11
- 11
Article Description
Mycobacterium avium complex is a causative organism for refractory diseases. In this study, we examined the effects of N-acetyl-cysteine on M. avium infection in vitro and in vivo. N-acetyl-cysteine treatment suppressed the growth of M. avium in A549 cells in a concentration-dependent manner. This effect was related to the induction of the antibacterial peptide human β-defensin-2. In a mouse model, N-acetyl-cysteine treatment significantly reduced the number of bacteria in the lungs and induced murine β-defensin-3. In interleukin-17-deficient mice, the effects of N-acetyl-cysteine disappeared, indicating that these mechanisms may be mediated by interleukin-17. Moreover, an additional reduction in bacterial load was observed in mice administered N-acetyl-cysteine in combination with clarithromycin. Our findings demonstrate the potent antimycobacterial effects of N-acetyl-cysteine against M. avium by inducing antimicrobial peptide, suggesting that N-acetyl-cysteine may have applications as an alternative to classical treatment regimens.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1286457920301507; http://dx.doi.org/10.1016/j.micinf.2020.08.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85090563602&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/32882411; https://linkinghub.elsevier.com/retrieve/pii/S1286457920301507; https://dx.doi.org/10.1016/j.micinf.2020.08.003
Elsevier BV
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