ArticleAntimicrobial agents and chemotherapy2007
Concanavalin A protects mice from a lethal inoculation of intragastric Klebsiella pneumoniae and reduces the induced liver damage.
Article in Antimicrobial agents and chemotherapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Structure-function and application of plant lectins in disease biology and immunity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2019Review
- Targeting the Immune System with Plant Lectins to Combat Microbial Infections.Frontiers in pharmacology · 2017Review
- Protection against Klebsiella pneumoniae using lithium chloride in an intragastric infection model.Antimicrobial agents and chemotherapy · 2015Article
- Protective effect of FTY720 on several markers of liver injury induced by concanavalin a in mice.Current therapeutic research, clinical and experimental · 2012Article
- Experimental phage therapy in treating Klebsiella pneumoniae-mediated liver abscesses and bacteremia in mice.Antimicrobial agents and chemotherapy · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intragastric inoculation of Klebsiella pneumoniae can cause invasive diseases, including necrosis of liver tissues and bacteremia. The effect of concanavalin A (ConA) on K. pneumoniae was tested. Pretreatment with ConA was able to protect mice from K. pneumoniae infection in an intragastric model. K. pneumoniae-induced mouse death and liver injury such as liver necrosis, as well as blood levels of aspartate aminotransferase and alanine aminotransferase, were inhibited in a dose-dependent manner by ConA. ConA administered intravenously as late as 24 h after K. pneumoniae inoculation was still protective. In an in vitro assay, ConA was able to bind K. pneumoniae cells directly and further agglutinate them but had no effect on their in vitro growth. Surveys of bacterial counts of ConA-treated mice revealed that the bacteria were eliminated effectively in both blood and liver tissues. Furthermore, the bactericidal activity of macrophages against K. pneumoniae was also enhanced in a dose-dependent manner by ConA in an in vitro culture. These data suggest that ConA is a potentially therapeutic agent for K. pneumoniae-induced liver infection.
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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.