ArticleThe Journal of experimental medicine2002
The contribution of accessory toxins of Vibrio cholerae O1 El Tor to the proinflammatory response in a murine pulmonary cholera model.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 109 citations in OpenAlex.
- Article
- Inflammation induced by the new lineage ofFrontiers in immunology · 2025Article
- TheScience signaling · 2020Article
- El Tor BiotypeFrontiers in immunology · 2019Article
- A live vaccine rapidly protects against cholera in an infant rabbit model.Science translational medicine · 2018Article
- Article
- A rare case of necrotizing fasciitis caused by Vibrio cholerae O8 in an immunocompetent patient.Wiener klinische Wochenschrift · 2016Article
- Mechanisms of inflammasome activation by Vibrio cholerae secreted toxins vary with strain biotype.Infection and immunity · 2015Article
- Vibrio cholerae MARTX toxin heterologous translocation of beta-lactamase and roles of individual effector domains on cytoskeleton dynamics.Molecular microbiology · 2015Article
- Article
- Vibrio cholerae-induced inflammation in the neonatal mouse cholera model.Infection and immunity · 2014Article
- Genomic versatility and functional variation between two dominant heterotrophic symbionts of deep-sea Osedax worms.The ISME journal · 2014Article
- The route less taken: pulmonary models of enteric Gram-negative infection.Pathogens and disease · 2014Review
- The β-prism lectin domain of Vibrio cholerae hemolysin promotes self-assembly of the β-pore-forming toxin by a carbohydrate-independent mechanism.The Journal of biological chemistry · 2014Article
- Construction and evaluation of V. cholerae O139 mutant, VCUSM21P, as a safe live attenuated cholera vaccine.PloS one · 2014Article
- Promotion of colonization and virulence by cholera toxin is dependent on neutrophils.Infection and immunity · 2013Article
- Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013Review
- Vibrio cholerae evades neutrophil extracellular traps by the activity of two extracellular nucleases.PLoS pathogens · 2013Article
- Induction of cytokines in different organs after intranasal inoculation of Campylobacter jejuni in mice.Gut pathogens · 2012Article
- Neutrophils are essential for containment of Vibrio cholerae to the intestine during the proinflammatory phase of infection.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The contribution of accessory toxins to the acute inflammatory response to Vibrio cholerae was assessed in a murine pulmonary model. Intranasal administration of an El Tor O1 V. cholerae strain deleted of cholera toxin genes (ctxAB) caused diffuse pneumonia characterized by infiltration of PMNs, tissue damage, and hemorrhage. By contrast, the ctxAB mutant with an additional deletion in the actin-cross-linking repeats-in-toxin (RTX) toxin gene (rtxA) caused a less severe pathology and decreased serum levels of proinflammatory molecules interleukin (IL)-6 and murine macrophage inflammatory protein (MIP)-2. These data suggest that the RTX toxin contributes to the severity of acute inflammatory responses. Deletions within the genes for either hemagglutinin/protease (hapA) or hemolysin (hlyA) did not significantly affect virulence in this model. Compound deletion of ctxAB, hlyA, hapA, and rtxA created strain KFV101, which colonized the lung but induced pulmonary disease with limited inflammation and significantly reduced serum titers of IL-6 and MIP-2. 100% of mice inoculated with KFV101 survive, compared with 20% of mice inoculated with the ctxAB mutant. Thus, the reduced virulence of KFV101 makes it a prototype for multi-toxin deleted vaccine strains that could be used for protection against V. cholerae without the adverse effects of the accessory cholera toxins.
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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.