ArticleInfection and immunity2005
Virulent Shigella flexneri causes damage to mitochondria and triggers necrosis in infected human monocyte-derived macrophages.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Legionella effector LpPIP recruits protein phosphatase 1 to the mitochondria to induce dephosphorylation of outer membrane proteins.PLoS biology · 2025Article
- Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021Review
- Reactive Oxygen Species: Not Omnipresent but Important in Many Locations.Frontiers in cell and developmental biology · 2021Article
- Mitochondrial Functions in Infection and Immunity.Trends in cell biology · 2020Review
- Mitochondrial Regulation of Macrophage Response Against Pathogens.Frontiers in immunology · 2020Review
- Human Enteric Defensin 5 PromotesInfection and immunity · 2019Article
- Interaction between Intracellular Bacterial Pathogens and Host Cell Mitochondria.Microbiology spectrum · 2019Review
- Role of Pyroptosis in Cardiovascular Diseases and its Therapeutic Implications.International journal of biological sciences · 2019Review
- A clinically parameterized mathematical model of Shigella immunity to inform vaccine design.PloS one · 2018Article
- Septins restrict inflammation and protect zebrafish larvae from Shigella infection.PLoS pathogens · 2017Article
- Characterization of a multicomponent live, attenuated Shigella flexneri vaccine.Pathogens and disease · 2016Article
- Macrophage Apoptosis Triggered by IpaD from Shigella flexneri.Infection and immunity · 2016Article
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- B lymphocytes undergo TLR2-dependent apoptosis upon Shigella infection.The Journal of experimental medicine · 2014Article
- Necroptosis: molecular signalling and translational implications.International journal of cell biology · 2014Review
- Intracellular Shigella remodels its LPS to dampen the innate immune recognition and evade inflammasome activation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Deubiquitinating enzymes as promising drug targets for infectious diseases.Current pharmaceutical design · 2013Review
- Applying mathematical tools to accelerate vaccine development: modeling Shigella immune dynamics.PloS one · 2013Article
- Programmed necrosis: backup to and competitor with apoptosis in the immune system.Nature immunology · 2011Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Shigella flexneri is a gram-negative bacterium that causes bacillary dysentery in humans that is characterized by an acute inflammatory response of the colon. The fate of phagocytes that are infected in vitro with virulent Shigella has been the subject of some investigation and debate. In this study we found that virulent Shigella caused a rapid increase in the cell membrane permeability of infected human monocyte-derived macrophages (HMDM) but not in the cell membrane permeability of monocytes, as demonstrated by the uptake of fluorescent vital dyes. Within 2 h of infection, 59% +/- 6% of the HMDM and </=4% of the monocytes were stained with propidium iodide. Treatment of the cells with the inhibitors of caspases YVAD and zVAD, the antioxidants N-acetyl-l-cysteine and butylated hydroxyanisole, or an inhibitor of NADPH oxidase, diphenyleniodonium, did not alter the infection outcome. Importantly, we found that virulent Shigella caused a rapid drop in the ATP level to about 50% in infected HMDM. Furthermore, using a combination of fluorescent vital dyes and mitochondrial membrane potential-sensitive dyes, we observed that cells that exhibited a permeable cell membrane were not stained by the mitochondrion-specific dyes, indicating that the mitochondrial membrane potential was lost in these cells. We also observed infected cells that were not stained with either type of dye, indicating that the loss of the mitochondrial membrane potential preceded the increase in cell membrane permeability. Taken together, our studies showed that virulent Shigella flexneri targets the host cell mitochondria for destruction. This activity may account for the necrotic cell death precipitated by these pathogens.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.