Disease relevance of Trichinella spiralis

• METHODS: Distal colitis was induced by intrarectal administration of trinitrobenzene sulfonic, acetic acid, or Trichinella spiralis larvae, or by intraperitoneal injection of mitomycin C [1].
• IL-18 regulates intestinal mastocytosis and Th2 cytokine production independently of IFN-gamma during Trichinella spiralis infection [2].
• However, during expulsion of Trichinella spiralis this Th2 response also induces a severe enteropathy characterized by villus atrophy and crypt hyperplasia [3].
• Transgene-encoded antiphosphorylcholine (T15+) antibodies protect CBA/N (xid) mice against infection with Streptococcus pneumoniae but not Trichinella spiralis [4].
• The effects of histamine and an antihistamine on Trichinella spiralis and on trichinous enteritis in the host [5].

High impact information on Trichinella spiralis

• Mebendazole was highly effective against the helminth parasite Trichinella spiralis in mice subjected to a 3-day course of treatment during the invasive and encystment phases of experimental trichinellosis [6].
• Delayed expulsion of the nematode Trichinella spiralis in mice lacking the mucosal mast cell-specific granule chymase, mouse mast cell protease-1 [7].
• To determine if the altered IFN-gamma regulation pattern and its immunological consequences would extend to a natural infection, we studied mice infected with the parasitic helminth Trichinella spiralis [8].
• Immunity to Trichinella spiralis infection in vitamin A-deficient mice [8].
• IgE antibody and resistance to infection. I. Selective suppression of the IgE antibody response in rats diminishes the resistance and the eosinophil response to Trichinella spiralis infection [9].

Chemical compound and disease context of Trichinella spiralis

• A thymus-independent (type 1) phosphorylcholine antigen isolated from Trichinella spiralis protects mice against pneumococcal infection [10].
• Effect of size of Trichinella spiralis (Nematode) infections on glucose and ion transport in the rat intestine [11].
• The effects of cortisone on fecundity, number, and distribution of adult Trichinella spiralis and on trichinous enteritis in the host [12].
• Oral administration of either Mebendazole or Fenbendazole at 50 mg/kg body weight was effective in killing a 7-hr Trichinella spiralis infection in mice [13].
• Antibodies against the less than 12-kD diagnostic antigen were detected in sera from 10 cattle and 4 swine inoculated with metacestodes of T saginata and T solium, respectively, but not in animals inoculated with Fasciola hepatica, Trichinella spiralis, Brucella abortus, or Toxoplasma gondii, or in noninoculated controls [14].

Biological context of Trichinella spiralis

• METHODS: Mice infected up to 70 days previously with Trichinella spiralis (Tsp) underwent videofluoroscopy with image analysis to assess upper gastrointestinal motility [15].
• We infected C57BL/6, athymic, CD4-deficient, CD8alpha-deficient, and major histocompatibility complex class II (MHC II)-deficient (C2d) mice with Trichinella spiralis larvae [16].
• Four homologs with differences at the purported active site histidine residue were detected in the parasitic nematodes Trichinella spiralis and Trichinella pseudospiralis [17].
• Serine/threonine protein kinase activity was identified in excretory/secretory (ES) products of Trichinella spiralis infective larvae, via phosphorylation of exogenous and endogenous substrates [18].
• The involvement of second messengers in the control of activation-induced changes to the surface of Trichinella spiralis infective larvae was investigated using membrane-permeant photo-activatable 'caged' compounds to alter intracellular levels of inositol trisphosphate (IP3), calcium ions (Ca2+) and cyclic AMP (cAMP) [19].

Anatomical context of Trichinella spiralis

• Because expulsion of another gastrointestinal nematode, Trichinella spiralis, unlike N. brasiliensis expulsion, is mast cell dependent, these observations suggested that T. spiralis expulsion would be Stat6 independent [20].
• ACh release from the myenteric plexus was measured in MHC II- and M-CSF-deficient (op/op) mice infected with Trichinella spiralis [21].
• Lymphocyte proliferation and cytokine production in mice infected with different geographical isolates of Trichinella spiralis [22].
• We analysed the cytokine profile of a T cell subset (CD4+ CD45 RC-) that confers protection against Trichinella spiralis infection in rats [23].
• Mice harbouring such infections were found to be less capable of responding to a primary infection with Trichinella spiralis or of producing humoral responses to lipopolysaccharide and sheep red blood cells [24].

Associations of Trichinella spiralis with chemical compounds

• BACKGROUND: A marked suppression of acetylcholine (ACh) release from myenteric nerves in the inflamed intestine of rats infected by Trichinella spiralis has been shown [25].
• This was associated with a reduction in the Trichinella spiralis -associated T-helper 2 response and a reduction in transforming growth factor-beta1, cyclooxygenase-2, and prostaglandin E 2 levels in muscle [26].
• Analysis of a 43-kDa glycoprotein from the intracellular parasitic nematode Trichinella spiralis [27].
• Nitric oxide mediates intestinal pathology but not immune expulsion during Trichinella spiralis infection in mice [28].
• Intestinal inflammation following Trichinella spiralis infection markedly downregulates NEP, resulting in diminished SP degradation, with unknown functional consequences [29].

Gene context of Trichinella spiralis

• Helminth regulation of host IL-4Ralpha/Stat6 signaling: mechanism underlying NOS-2 inhibition by Trichinella spiralis [30].
• Stat6 signaling promotes protective immunity against Trichinella spiralis through a mast cell- and T cell-dependent mechanism [20].
• Treatment of mice with recombinant interleukin-3 (rIL-3) accelerated an IL-4-dependent IgE production following infection with Trichinella spiralis [31].
• What is the role of p53 during the cyst formation of Trichinella spiralis ? A comparable study between knockout mice and wild type mice [32].
• In order to reveal the mechanisms underlying nurse cell formation during Trichinella spiralis infection, the expression of the factors of tumor necrosis factor-alpha (TNF-alpha)/TNF receptor 1 (TNFR-1) signalling pathway mediating apoptosis was investigated [33].

Analytical, diagnostic and therapeutic context of Trichinella spiralis

• Molecular cloning and characterization of a serine proteinase inhibitor from Trichinella spiralis [34].
• Oral and parenteral vaccination against Trichinella spiralis infections in high- and low-responder mice [35].
• The diagnosis was made by demonstration of larvae of Trichinella spiralis in the muscle biopsy and also by the presence of anti-Trichinella antibodies detected by double immunodiffusion in their sera [36].
• In avidin-based ELISA using antinematode monoclonal antibodies, an extract of the nematode Anisakis simplex showed very high background reactivity due to biotin/BCMs, whereas the background reactivity in an extract of the nematode Trichinella spiralis was negligible [37].
• Changes in the activity of glutathione-S-transferase in muscles and sera from mice infected with Trichinella spiralis after treatment with albendazole and levamisole [38].

References