ArticleParasitology research2004
Kinetics of change in the eotaxin concentration in serum and cerebrospinal fluid of mice infected with Angiostrongylus cantonensis.
Article in Parasitology research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 18 citations in OpenAlex.
- Cytokines in the Brain and Neuroinflammation: We Didn't Starve the Fire!Pharmaceuticals (Basel, Switzerland) · 2022Review
- Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection.Parasites & vectors · 2015Article
- AcCystatin, an immunoregulatory molecule from Angiostrongylus cantonensis, ameliorates the asthmatic response in an aluminium hydroxide/ovalbumin-induced rat model of asthma.Parasitology research · 2015Article
- Eosinophil chemotactic chemokine profilings of the brain from permissive and non-permissive hosts infected with Angiostrongylus cantonenis.Parasitology research · 2014Article
- Differences of larval development and pathological changes in permissive and nonpermissive rodent hosts for Angiostrongylus cantonensis infection.Parasitology research · 2012Article
- Kinetic change of oxidative stress in cerebrospinal fluid of mice infected with Angiostrongylus cantonensis.Redox report : communications in free radical research · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kinetics of changes in the eotaxin concentration in the serum and cerebrospinal fluid (CSF) of BALB/c mice after infection with Angiostrongylus cantonensis and the correlation between the concentration of eotaxin and worm recovery were investigated. The mean concentration of eotaxin in serum of infected mice gradually increased from 46.3+/-6.5 pg/ml at week 0 to 104.9+/-44.8 pg/ml at week 3 after infection, while the mean eotaxin level in the CSF of infected mice rapidly increased from 18.7+/-2.1 pg/ml to 193.2+/-23.6 pg/ml 1 week after infection and then increased further to 507.8+/-167.9 pg/ml at week 3. The concentrations of eotaxin in the CSF of infected mice each week after infection were all significantly higher than those in serum ( P<0.0001). In parallel with the increase in eotaxin in the CSF, infected mice showed gradual increases in CSF eosinophilia and a reduction in intracranial worm recovery. The concentration of eotaxin in CSF was higher in infected mice with more worms in the brain, except when the number of worms in the brain was >30. In addition, when the worm counts in the brains of infected mice were <30, eotaxin concentrations in the CSF were positively correlated with worm counts in the brain ( P<0.001). Thus, the release of eotaxin in the CSF of mice infected with A. cantonensis observed in this study was time dependent and worm-load dependent, and in parallel with the increase in eotaxin in the CSF, and gradual decreases in worm counts in the brains of infected mice.
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