This study investigated the presence of cytokines interferon (IFN)-gamma, interleukins (IL) -6 and -8 in serum of cattle and buffaloes infected with Fasciola gigantica from one to 16 weeks post-infection to determine their T cell response during infection. The concentration of these cytokines was determined by sandwich enzyme-linked immunosorbent assay (ELISA). No IFN-gamma was detected in these animals while IL-6 was elevated from one to 16 weeks postinfection. Levels of IL-8 were also elevated in infected buffaloes from one to 16 weeks post-infection. A predominantly T helper (Th) 2 response which started early in the infection was apparently present in cattle and buffaloes in this study which was characterised by IL-6. IL-8 production could be another mechanism of immune response in buffaloes during infection with F. gigantica.
Animals ; Buffaloes/blood/immunology/*parasitology ; Cattle ; Cattle Diseases/*immunology/*parasitology ; Cytokines/*blood/immunology ; Enzyme-Linked Immunosorbent Assay/veterinary ; Fasciola/*immunology ; Fascioliasis/immunology/parasitology/*veterinary ; Interferon Type II/blood ; Interleukin-6/blood ; Interleukin-8/blood ; Random Allocation

In order to investigate cytokine productions in patients undergoing continuous ambulatory peritoneal dialysis (CAPD), we studied the production of interleukin (IL)-1 beta, -6 and interferon (IFN)-gamma by cultured peripheral blood mononuclear cells (PBMC) in peritonitis-free CAPD patients. The correlation of cytokine production with plasma parathyroid hormone (PTH) and albumin levels was also evaluated. While the release of IL-1 beta was not markedly different from controls release of IL-6 from 24-hour cultured PBMCs was significantly greater than that of controls, (Mean +/- S.D., IL-6: 2186.8 +/- 1217.9 pg/ml, vs 1516.3 +/- 767.9, P <0.05). The addition of lipopolysaccharide (LPS, 10 micrograms/ml, significantly stimulated IL-1 beta and -6 production of PBMCs in CAPD patients and controls, compared to an unstimulated condition. The LPS-induced IL-1 beta production was also not markedly different from controls, whereas LPS-induced IL-6 production was significantly higher than controls (IL-6: 13,220.7 +/- 7177.4 vs 7411.4 +/- 1236.9, P <0.05). However, the percentage increases of IL-6 production stimulated with LPS in CAPD patients were not significantly different from controls (p > 0.05). No difference of baseline IFN-gamma was detected between CAPD patients controls, but phytohemagglutinin (PHA, 10 micrograms/ml)-stimulated IFN-gamma release was significantly higher in CAPD patients than controls (2425.9 +/- 1565.0 pg/ml vs 1364.0 +/- 755.1, P <0.05). There was no significant correlation between PTH and, IL-1 beta, serum albumin level and LPS-stimulated IL-6 production (r = 0.54, P <0.05). In conclusion, CAPD seems to partly induce activation of PBMCs with an enhanced release of IL-6 and IFN-gamma, and CAPD patients with higher serum albumin levels tend to show higher IL-6 production in immune response.
Adult ; Cells, Cultured ; Female ; Human ; Interferon Type II/biosynthesis* ; Interleukin-1/biosynthesis* ; Interleukin-6/biosynthesis* ; Male ; Middle Age ; Monocytes/metabolism ; Parathyroid Hormones/blood ; Peritoneal Dialysis, Continuous Ambulatory* ; Serum Albumin/analysis

Regulatory T cells, which stimulate or inhibit the effector functions of distinct T cell subsets, are critical in the control of the immune response. We investigated the effect of TGF-beta and IL-10 on T cell subsets according to the Th1/Th2 immune status. Sixty-two patients with asthma and 38 patients with pulmonary tuberculosis were included. Allergy skin tests, tuberculin tests, and chest radiography were performed. The levels of circulating IL-4, IFN-gamma, TGF-beta1, and IL-10 were measured using ELISA. The level of TGF-beta1 was higher in patients with asthma than in those with tuberculosis, but the IL-10 levels were the same between the asthma and tuberculosis groups. Atopy was unrelated to the tuberculin response. The IFN-gamma level was correlated with the IL-10 level, and the level of IL-4 was unrelated to the IL-10 or TGF-beta1 level. The level of IL-10 was higher in the negative tuberculin reactors than in the positive tuberculin reactors among patients with asthma, and TGF-beta1 was higher in the positive tuberculin reactors than in the negative tuberculin reactors among patients with tuberculosis. These results demonstrate that the regulatory effects of circulating TGF-beta and IL-10 on T cell cytokines may be different between Th2-type asthma and Th1 tuberculosis.
Adult ; Asthma/*blood/immunology ; Cytokines/*blood ; Female ; Humans ; Interferon Type II/blood ; Interleukin-10/blood ; Interleukin-4/blood ; Male ; Research Support, Non-U.S. Gov't ; Respiratory Function Tests ; Skin Tests ; Th1 Cells/*metabolism ; Th2 Cells/*metabolism ; Transforming Growth Factor beta/blood ; Tuberculin Test ; Tuberculosis/*blood/immunology

OBJECTIVETo investigate the effects of oral administration of type II collagen (CII) on adjuvant arthritis (AA) in rats and its mechanisms, and to compare the effects of CII with those of the Chinese traditional medicine Tripterygium Polyglycoside administered similarly.

METHODSArthritis was induced in rats by immunization using Freund's complete adjuvant (FCA). After feeding rats either soluble CII or Tripterygium Polyglycoside, changes in degree of articular swelling and articular histological findings were observed in AA rats. Some correlative immunological indexes were measured, including delayed type hypersensitivity (DTH) reaction, anti-collagen and anti-Mycobacterium tuberculosis (MT) antibody in serum, and levels of IFN-gamma and TNF-alpha in articular steep in rats.

RESULTSOral administration of CII was able to alleviate both distinctly articular and general symptoms in AA rats, suppress synovium hyperplasia and inflammatory cells infiltration in arthrosis capsule. The effects brought about by CII were stronger than those by Tripterygium Polyglycoside. Oral administration of CII inhibited antigen-specific immune response, such as DTH and antibody reaction to CII. In addition, the expression of IFN-gamma and TNF-alpha in joints were locally downregulated.

CONCLUSIONSThe therapeutic effect of oral administration of CII is obvious on adjuvant arthritis in rats. Its remedial mechanisms are likely related to the downregulation of both IFN-gamma and TNF-alpha, and the suppression of cell immunity.

Administration, Oral ; Animals ; Antibodies ; blood ; Arthritis, Experimental ; drug therapy ; immunology ; Collagen Type II ; therapeutic use ; Hypersensitivity, Delayed ; prevention & control ; Immune Tolerance ; Interferon-gamma ; biosynthesis ; Male ; Mycobacterium tuberculosis ; immunology ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Synovial Membrane ; pathology ; Tripterygium ; Tumor Necrosis Factor-alpha ; biosynthesis

Food allergies affect about 4% of the Korean population, and buckwheat allergy is one of the most severe food allergies in Korea. The purpose of the present study was to develop a murine model of IgE-mediated buckwheat hypersensitivity induced by intragastric sensitization. Young female C3H/HeJ mice were sensitized and challenged intragastricly with fresh buckwheat flour (1, 5, 25 mg/dose of proteins) mixed in cholera toxin, followed by intragastric challenge. Anaphylactic reactions, antigen-specific antibodies, splenocytes proliferation assays and cytokine productions were evaluated. Oral buckwheat challenges of sensitized mice provoked anaphylactic reactions such as severe scratch, perioral/periorbital swellings, or decreased activity. Reactions were associated with elevated levels of buckwheatspecific IgE antibodies. Splenocytes from buckwheat allergic mice exhibited significantly greater proliferative responses to buckwheat than non-allergic mice. Buckwheat-stimulated IL-4, IL-5, and INF-gamma productions were associated with elevated levels of buckwheat-specific IgE in sensitized mice. In this model, 1 mg and 5 mg dose of sensitization produced almost the same degree of Th2-directed immune response, however, a 25 mg dose showed blunted antibody responses. In conclusion, we developed IgE-mediated buckwheat allergy by intragastric sensitization and challenge, and this model could provide a good tool for future studies.
Anaphylaxis/blood/immunology ; Animals ; Cell Proliferation/drug effects ; Comparative Study ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Enzyme-Linked Immunosorbent Assay ; Fagopyrum/*immunology ; Female ; *Flour ; Food Hypersensitivity/blood/*immunology ; Immunoglobulin E/blood/immunology ; Immunoglobulin G/blood/immunology ; Interferon Type II/biosynthesis ; Interleukin-4/biosynthesis ; Interleukin-5/biosynthesis ; Mice ; Mice, Inbred C3H ; Plant Extracts/administration & dosage/immunology ; Research Support, Non-U.S. Gov't ; Spleen/cytology/drug effects/metabolism ; Stomach/drug effects/*immunology ; T-Lymphocytes/cytology/drug effects/metabolism ; Time Factors