ArticleParasitology research2008
The effectors responsible for gastrointestinal nematode parasites, Trichinella spiralis, expulsion in rats.
Article in Parasitology research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 22 citations in OpenAlex.
- Cellular and molecular changes and immune response in the intestinal mucosa during Trichinella spiralis early infection in rats.Parasites & vectors · 2020Article
- Changes in Epithelial Barrier Function in Response to Parasitic Infection: Implications for IBD Pathogenesis.Journal of Crohn's & colitis · 2015Article
- Taurine drinking attenuates the burden of intestinal adult worms and muscle larvae in mice with Trichinella spiralis infection.Parasitology research · 2013Article
- Coinfection with Clonorchis sinensis modulates murine host response against Trichinella spiralis infection.Parasitology research · 2013Article
- Construction and use of a Trichinella spiralis phage display library to identify the interactions between parasite and host enterocytes.Parasitology research · 2013Article
- The different infectivity of Trichinella spiralis and Trichinella nativa in rat does not solely localize to enteral or parenteral phase.Parasitology research · 2012Article
- Cryptosporidium parvum isolate-dependent postinfectious jejunal hypersensitivity and mast cell accumulation in an immunocompetent rat model.Infection and immunity · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helper T (Th2) cells type 2 have a central role in host protective responses to gastrointestinal nematode parasite, Trichinella spiralis infection, but the actual effector mechanisms involved in parasite expulsion are still uncertain. Recent evidences suggest that mast cell recruitment and activation may associate with parasite elimination from host intestines in mice. On the other hand, IgE production may induce defensive responses to primary infection with the helminth in rats. The differences of host effector mechanisms to the same experimental infections might disturb our understanding of the host protective mechanisms to gastrointestinal nematode parasite infection. In order to redefine these differences, we investigated in detail the relationship between intestinal immune responses and worm expulsion following T. spiralis infection among several rat strains including mutants. As a result, there were significant correlations of parasite expulsion with mast cell hyperplasia in addition to serum IgE level. Moreover, mast cell-deficient and dysfunction rats showed delayed worm elimination from their gut. Therefore, the present study suggests that mast cells should also be one of the prominent effector cells involved in T. spiralis parasite expulsion in rats as well as mice.
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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.