ArticlePLoS pathogens2023
Mycobacterium abscessus resists the innate cellular response by surviving cell lysis of infected phagocytes.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
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- Genome-wide phenotypic insights into mycobacterial virulence using Drosophila melanogaster.PLoS pathogens · 2025Article
- An alveolus lung-on-a-chip model of Mycobacterium fortuitum lung infection.Disease models & mechanisms · 2025Article
- An alveolus lung-on-a-chip model ofbioRxiv : the preprint server for biology · 2025Article
- Insights on the Pathogenesis ofJournal of clinical medicine · 2025Review
- In Vitro Activity of Imipenem/Relebactam Alone and in Combination Against Cystic Fibrosis Isolates ofAntibiotics (Basel, Switzerland) · 2025Article
- ENaC is a host susceptibility factor to bacterial infections in cystic fibrosis context.Communications biology · 2025Article
- Harnessing hypoxia: bacterial adaptation and chronic infection in cystic fibrosis.FEMS microbiology reviews · 2025Review
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- Insights intoFrontiers in cellular and infection microbiology · 2025Article
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- Ouabain alleviatesFrontiers in immunology · 2025Article
- Remote disruption of intestinal homeostasis by Mycobacterium abscessus is detrimental to Drosophila survival.Scientific reports · 2024Article
- Microbial metabolism disrupts cytokine activity to impact host immune response.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- When the microbiome shapes the host: immune evolution implications for infectious disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Review
- Mycobacterium abscessus Opsonization Allows an Escape from the Defensin Bactericidal Action inMicrobiology spectrum · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium abscessus is the most pathogenic species among the predominantly saprophytic fast-growing mycobacteria. This opportunistic human pathogen causes severe infections that are difficult to eradicate. Its ability to survive within the host was described mainly with the rough (R) form of M. abscessus, which is lethal in several animal models. This R form is not present at the very beginning of the disease but appears during the progression and the exacerbation of the mycobacterial infection, by transition from a smooth (S) form. However, we do not know how the S form of M. abscessus colonizes and infects the host to then multiply and cause the disease. In this work, we were able to show the hypersensitivity of fruit flies, Drosophila melanogaster, to intrathoracic infections by the S and R forms of M. abscessus. This allowed us to unravel how the S form resists the innate immune response developed by the fly, both the antimicrobial peptides- and cellular-dependent immune responses. We demonstrate that intracellular M. abscessus was not killed within the infected phagocytic cells, by resisting lysis and caspase-dependent apoptotic cell death of Drosophila infected phagocytes. In mice, in a similar manner, intra-macrophage M. abscessus was not killed when M. abscessus-infected macrophages were lysed by autologous natural killer cells. These results demonstrate the propensity of the S form of M. abscessus to resist the host's innate responses to colonize and multiply within the host.
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