epiglucan has been researched along with Immune-System-Diseases* in 3 studies
3 other study(ies) available for epiglucan and Immune-System-Diseases
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Clinical Value of sTREM-1, PCT, and 1,3-
Fungal infection in the lungs can cause fungal infectious diseases. This disease develops rapidly and involves a wide range. Pathogenic fungi are also more serious types of pathogenic bacteria. If it invades deep organs and tissues, it will endanger life, so it needs timely diagnosis.. To investigate the diagnostic value of serum soluble myeloid cell triggering receptor-1 (sTREM-1), procalcitonin (PCT), and 1,3-. In this study, a case-control study was conducted. 50 patients with immune-related pulmonary disease complicated with fungal infection (infection group) diagnosed by sputum culture in our hospital from January 2017 to December 2021 were selected as the control group, and 50 patients with immune-related pulmonary disease without fungal infection were selected as the control group. The levels of sTREM-1, PCT, and 1,3-. The levels of sTREM-1, PCT, and 1,3-. The detection of sTREM-1, PCT, and 1,3- Topics: beta-Glucans; Biomarkers; C-Reactive Protein; Case-Control Studies; Humans; Immune System Diseases; Lung; Lung Diseases; Mycoses; Myeloid Cells; Procalcitonin; Prospective Studies; Triggering Receptor Expressed on Myeloid Cells-1 | 2022 |
Curdlan oligosaccharides having higher immunostimulatory activity than curdlan in mice treated with cyclophosphamide.
This study evaluated the immunostimulatory activity of curdlan oligosaccharides (GOS) in cyclophosphamide (CTX)-induced immunosuppressed mice and in RAW264.7 cells. GOS was able to stimulate the release of nitric oxide (NO), cytokines (IL-1β, IL-6 and TNF-α) and improve the phagocytic rate of peritoneal macrophages and RAW264.7 cells. It further enhanced immunoglobulins (Ig) release (IgG by 50.6%-74.7%, IgA by 31.3%-34.9%, IgM by 28.3%-66.7%), splenic lymphocyte proliferation (by 74.8%-91.3%), nature killer cells cytotoxicity (by 32.0%-49.6%), immunophenotypes of splenic lymphocytes (from 1.7 to 2.4, 2.2 and 2.7) in immunosuppressed mice. Compared with curdlan, higher immunostimulatory activity of GOS was found in CTX-treated mice. Moreover, GOS could activate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways through toll-like receptor 2 (TLR2) and complement receptor 3 (CR3). These results indicated that GOS may be a favorable candidate of functional food in regulating immune responses. Topics: Adjuvants, Immunologic; Administration, Oral; Alcaligenes; Animals; beta-Glucans; Body Weight; Cyclophosphamide; Cytokines; Immune System Diseases; Immunity, Humoral; Immunosuppression Therapy; Killer Cells, Natural; Macrophages; Male; MAP Kinase Signaling System; Mice; Mice, Inbred BALB C; Oligosaccharides; RAW 264.7 Cells; T-Lymphocytes | 2019 |
Association of immunological disorders in lethal side effect of NSAIDs on beta-glucan-administered mice.
(1-->3)-beta-D-Glucan (beta-glucan) is a biological response modifier that regulates host immune response. We have found that the combination of a beta-glucan and a non-steroidal anti-inflammatory drug (NSAID), indomethacin (IND), induced lethal toxicity in mice [Yoshioka et al. (1998) FEMS Immunol. Med. Microbiol., 21, 171-179]. This study was undertaken to analyze the mechanism of the lethal side effect. Combination of a beta-glucan and IND increased the number of leukocytes, especially macrophages and neutrophils, in various organs and these cells were activated. The activated state of these cells was supported by the enhanced production of interferon-gamma in the presence of IND in vitro culture of the peritoneal exudate cells. Intestinal bacterial flora was translocated into the peritoneal cavity in these mice to cause peritonitis. Comparing the toxicity of various NSAIDs, nabumetone, a partially cyclooxygenase-2-selective NSAID with weaker toxicity to the gastrointestinal tract, did not exhibit a lethal side effect. These facts strongly suggested that gastrointestinal damage by NSAIDs was more severe in beta-glucan-administered mice, resulting in peritonitis by enteric bacteria and leading to death. Topics: Administration, Oral; Animals; Anti-Inflammatory Agents, Non-Steroidal; beta-Glucans; Butanones; Colony Count, Microbial; Glucans; Immune System Diseases; Immunologic Factors; Indomethacin; Leukocyte Count; Leukocytes; Liver; Macrophages; Male; Mice; Mice, Inbred ICR; Mice, Inbred Strains; Nabumetone; Neutrophils; Peritonitis; Specific Pathogen-Free Organisms; Spleen | 2001 |