Disease relevance of Nippostrongylus

• Here, we show that in the absence of CD28 both T helper cell type 1 (Th1) and Th2 responses were impaired but not abrogated after infection with lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and the nematode Nippostrongylus brasiliensis [1].
• The effect of methionine and protein deficiency in delaying expulsion of Nippostrongylus brasiliensis in the rat [2].
• A new method for the in vitro generation of granulomas was developed and characterized in which L3 larvae of Nippostrongylus brasiliensis, as a target for the cellular response, were co-incubated with human mononuclear blood cells [3].
• SCID(T) and SCID(T + B) mice were infected with the nematode parasite Nippostrongylus brasiliensis and analyzed for the development of IL-5-dependent peripheral blood eosinophilia [4].
• Recent studies have shown that bilateral decentralization (sympathectomy) of the superior cervical ganglia (SCG) of rats sensitized to the parasite Nippostrongylus brasiliensis attenuated the development of pulmonary inflammation following allergen challenge [5].

High impact information on Nippostrongylus

• In the absence of B and T cells, IL-4-expressing eosinophils were recruited to tissues of mice infected with the helminth Nippostrongylus brasiliensis, but eosinophils failed to degranulate [6].
• Eosinophil chemotactic factor release from neutrophils by Nippostrongylus brasiliensis larvae [7].
• IL-13, IL-4Ralpha, and Stat6 are required for the expulsion of the gastrointestinal nematode parasite Nippostrongylus brasiliensis [8].
• Unexpectedly, challenge of these mice with Nippostrongylus brasiliensis, a Th2-inducing stimulus, failed to result in the development of Th2 cells [9].
• In vivo deletion of Gata3 using OX40-Cre eliminated T(H)2 responses and allowed the development of interferon-gamma-producing cells in mice infected with Nippostrongylus brasiliensis [10].

Chemical compound and disease context of Nippostrongylus

• The potentiation effect of various adjuvants on the production of guinea-pig IgE was investigated using Freund's complete and incomplete adjuvant, the lipopolysaccharide of Escherichia coli and Salmonella typhosa, Bordetella pertussis, and the nematodes Nippostrongylus brasiliensis and Ascaris suum [11].
• Thiazoline and oxazoline analogues of the natural product mycothiazole were synthesized from a common intermediate and evaluated in vitro against HCT-15 colon cancer cells and L(4) larvae of nematode Nippostrongylus brasiliensis [12].
• Three infection models namely an oncogenic virus Encephalomyocarditis (EMCV), a rodent strain of malaria, Plasmodium berghei, and a rodent hookworm parasite, Nippostrongylus brasiliensis, were used to confirm the in vivo immunotoxic potential of styrene reported in our previous communication [13].
• The Nippostrongylus brasiliensis-rat model was used to determine whether iron and protein deficiency, which are commonly associated with parasitic infections, affected the pharmacokinetic behaviour of fenbendazole as measured by plasma concentrations and uptake by worms [14].

Biological context of Nippostrongylus

• Use of hydrogen gas (H2) analysis to assess intestinal absorption. Studies in normal rats and in rats infected with the nematode, Nippostrongylus brasiliensis [15].
• Up-regulation was also found for E-selectin ligands during influenza, but not Nippostrongylus infection [16].
• Identification of transient glycosylation alterations of sialylated mucin oligosaccharides during infection by the rat intestinal parasite Nippostrongylus brasiliensis [17].
• Cysteine protease of the nematode Nippostrongylus brasiliensis preferentially evokes an IgE/IgG1 antibody response in rats [18].
• The Indian soft-furred rat, Millardia meltada, a new host for Nippostrongylus brasiliensis, showing androgen-dependent sex difference in intestinal mucosal defence [19].

Anatomical context of Nippostrongylus

• Infection of Nippostrongylus brasiliensis induces normal increase of basophils in mast cell-deficient Ws/Ws rats with a small deletion at the kinase domain of c-kit [20].
• An injection of 0.2 mg dexamethasone into rats infected with Nippostrongylus brasiliensis markedly diminished the proportion of Fc epsilon R(+) lymphocytes in their mesenteric lymph nodes [21].
• By 14 days after Nippostrongylus brasiliensis infection, the level of Fc epsilon RII increased on B lymphocytes located in the cortex of draining mesenteric lymph nodes [22].
• Antigenic challenge of Nippostrongylus brasiliensis-infected mice induces a striking increase in histidine decarboxylase (HDC) activity in both spleen and bone marrow cells [23].
• The secretory activity of peritoneal mast cells was studied in vitro after challenge with compound 48/80 of cells obtained from normal rats and with anti-rat IgE of cells obtained from rats hyperimmunised with Nippostrongylus brasiliensis [24].

Associations of Nippostrongylus with chemical compounds

• T1/ST2(-/-) mice showed normal Th2 responses after infection with the helminthic parasite Nippostrongylus brasiliensis as well as in the mouse model of allergen-induced airway inflammation [25].
• Rats previously infected with Nippostrongylus brasiliensis received a single IP injection of 1 mg dexamethasone [26].
• Rats infected with the helminth Nippostrongylus brasiliensis were injected i.p. with 2 mCi of [35S] sulfate on days 13, 15, 17, and 19 after infection [27].
• The benzimidazole anthelmintics mebendazole and fenbendazole have been shown to be much less effective against Nippostrongylus brasiliensis infections in the rat on a combined iron and protein deficient diet [28].
• In the absence of phosphatidylserine, NGF (1 ng/ml to 1 microgram/ml) did not cause histamine release from PMCs isolated from normal rats and those infected with the nematode Nippostrongylus brasiliensis [29].

Gene context of Nippostrongylus

• Although IL-4 induces expulsion of the gastrointestinal nematode parasite, Nippostrongylus brasiliensis, from immunodeficient mice, this parasite is expelled normally by IL-4-deficient mice [8].
• Injection of a mixture of IL-12 and IL-18 into mice inoculated with Nippostrongylus brasiliensis or injected with anti-IgD induced IFN-gamma-producing cells that inhibit IgE production in them [30].
• The lack of IL-4Ralpha resulted in markedly diminished, but not absent, TH2 responses after infection with the helminthic parasite Nippostrongylus brasiliensis [31].
• Moreover, MCP-5 expression was up-regulated in the lungs of mice following aerosolized antigen challenge of sensitized mice, and during the host response to infection with Nippostrongylus brasiliensis [32].
• Effects on polyclonal Ig production were tested in a Th2 cell-driven immune response in vivo after infection with Nippostrongylus brasiliensis, a parasite that dramatically enhances CD23 expression on B cells [33].

Analytical, diagnostic and therapeutic context of Nippostrongylus

• Mesenteric lymph node cells from normal rats and rats infected with Nippostrongylus brasiliensis (Nb) were cultured with pokeweed mitogen (PWM) or Nb antigen, and the development of IgM-, IgG2a-, or IgE-containing cells was assessed by immunofluorescence [34].
• To clarify the allergenicity of nematode cysteine proteases, the enzyme was purified from the intestinal nematode Nippostrongylus brasiliensis using cation exchange chromatography and gel filtration chromatography [18].
• A gamma-aminobutyric acid transferase (4-aminobutyrate:2-oxoglutarate aminotransferase; EC 2.6.1.19) preparation from Nippostrongylus brasiliensis was found to contain only one peak of enzyme activity with a highly basic pI of 10.5 when analysed by isoelectric focusing and chromatofocusing [35].
• The activity of the gluconeogenic enzyme, alanine-amino-transferase (ALT), in a preparation from the liver of rats was studied by means of an in vitro assay throughout the course of a primary infection of Nippostrongylus brasiliensis, established by a subcutaneous injection of approximately 4000 3rd-stage larvae [36].

References