ArticleParasitology research2011
Toxocara canis larvae reinfecting BALB/c mice exhibit accelerated speed of migration to the host CNS.
Article in Parasitology research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Neurobehavioral Disorders and Pathological Changes in the Brain of Mice Are Caused by Chronic Toxocara canis Larval Invasion with Low to Moderate Inoculum.Acta parasitologica · 2024Article
- Organ-specific Toxocara canis larvae migration and host immune response in experimentally infected mice.Parasites, hosts and diseases · 2024Article
- Larva migrans in BALB/c mice experimentally infected with Toxocara cati ensured by PCR assay.BMC veterinary research · 2022Article
- Article
- Toxocara canis mucins among other excretory-secretory antigens induce in vitro secretion of cytokines by mouse splenocytes.Parasitology research · 2015Article
- Neurotoxocarosis alters myelin protein gene transcription and expression.Parasitology research · 2015Article
- Toxocara canis: molecular basis of immune recognition and evasion.Veterinary parasitology · 2013Article
- Signal transducer and activator of transcription factor 6 signaling contributes to control host lung pathology but favors susceptibility against Toxocara canis infection.BioMed research international · 2013Article
- The 33.1 kDa Excretory/secretory Protein Produced byIranian journal of parasitologyArticle
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using a small animal imaging system, migratory activity of Toxocara canis larvae stained by carboxyfluorescein succinimidyl ester (CFSE) was observed post primary infection (PPI) and post reinfection (PR) of BALB/c mice. Each infection was performed with 1,000 larvae per mouse. Primary infections were performed with labeled larvae, while for challenge infections the reinfecting larvae were stained by CFSE. The worm burden in mouse organs was determined during a period from 6 h to 21 days and 4 months PPI and PR. In comparison with primary infections that led to the first larvae appearance in the brain after 60 h, greatly accelerated migration of the parasites administered 3 weeks PPI to the CNS and eyes of challenged mice was noted-in both organs the larvae appeared 6 h PR. In all challenged mice, reinfecting larvae prevailed in the resident parasite population. Preliminary experiments with Toxocara cati larvae also revealed early brain involvement in primarily infected mice. Staining of T. canis larvae by CFSE had no effect on the development of a humoral antibody response against T. canis excretory-secretory antigens. In ELISA, elevated levels of specific IgG and IgG1 were noted on day 14 PPI and the levels of antibodies increased till the end of experiment. Reinfection induced an increase in the levels of both antibodies. In terms of optical density, IgG1 antibodies gave higher values in all sera examined. In ELISA for IgG antibodies, an increase in the avidity index of around 50% was detected 1 month PPI; higher-avidity antibodies were also detected in sera of reinfected animals.
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