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Objective: To observe the effect of Guizhi Decoction (GZD) on immunological indexes in intestinal mucosal immune system of mice with Bi syndrome (collagen induced immune arthritis).
Methods: Eighty male DBA mice were randomly divided into 4 groups, the normal group, the model group and the high and low dosage GZD groups. Model of Bi syndrome was induced by collagen type II. CD4+, CD8+ T-lymphocytes and SIgA in mice' small intestine and PP node were labeled by immunohistochemical staining and their number was calculated using imaging analyzer.
Results: Compared with the normal group, in the model group, after immunization with collagen type II, numbers of CD4+ and CD8+ T-lymphocytes and SIgA in mice' intestinal mucosal immune system reduced significantly (P < 0.05 or P < 0.01). After treatment with GZD of both high and low dosage, CD4+ T-lymphocytes and SIgA increased significantly, but significant difference only showed in comparison between the high dosage GZD group and the model group (P < 0.05 or P < 0.01).
Conclusion: GZD could enhance the immune function in intestinal mucosa in mice with Bi syndrome, thus it might induce immune tolerance and immune inhibition.
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Proc Natl Acad Sci U S A
July 2025
Department of Microbiology and Immunology, University of British Columbia, Vancouver V6T 1Z3, BC, Canada.
The gut microbiota is highly dynamic during the first year of life and plays a crucial role in immune development. Breastfeeding is known to support infant health, but the contributions of the numerous breastmilk components to gut microbiota and immune maturation remain unclear. Secretory IgA (SIgA), the most abundant antibody in human milk, is a key modulator of gut microbiota composition.
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May 2025
Office of Pharmaceutical Quality Research, Center for Drug Evaluation and Research, U.S. Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, United States.
Several human lymphocyte subsets express the novel secretory IgA receptor FCRL3 (Fc receptor-like 3). Secretory IgA binding to FCRL3 diminishes the inhibitory capacity of regulatory T cells and promotes a T helper 17-like phenotype. Here, we report that in CD4+ regulatory T cells and CD8+ terminal effector T cells secretory IgA induced a shared inflammatory gene signature that included PTGS2 encoding COX2, and the prototypic inflammatory cytokine genes IL1A, IL1B, and IL8.
View Article and Find Full Text PDFCell Host Microbe
December 2024
IRCCS Humanitas Research Hospital, Via Manzoni 56, Rozzano, Milan 20089, Italy; Department of Biomedical Sciences, Humanitas University, Via Rita Levi Montalcini, Pieve Emanuele, Milan 20072, Italy. Electronic address:
Cell Rep
October 2024
Department of Microbiology & Immunology, University of British Columbia, Vancouver, BC V6T 1Z4, Canada; Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada; Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC V6T 1Z4,
Asthma susceptibility is linked to dysbiosis in early-life gut microbiota, and the antibody secretory immunoglobulin (Ig)A (SIgA) is a key determinant of gut microbiota composition. SIgA is obtained through breast milk during the critical early-life window. We use a mouse model of SIgA deficiency and the house dust mite (HDM) model of asthma to elucidate the role of maternal SIgA in modulating the early-life gut microbiota and asthma protection.
View Article and Find Full Text PDFPhytomedicine
October 2024
College of Veterinary Medicine, Northeast Agricultural University, 600 Changjiang Road, Xiangfang District, Harbin 150030, PR China; Heilongjiang Key Laboratory for Animal Disease Control and Pharmaceutical Development, 600 Changjiang Road, Xiangfang District, Harbin 150030, PR China. Electronic add
Background: Mycoplasma gallisepticum (MG) has long been a pathogenic microorganism threatening the global poultry industry. Previous studies have demonstrated that the mechanism by which quercetin (QUE) inhibits the colonization of MG in chicks differs from that of antibiotics. However, the molecular mechanism by which QUE facilitates the clearance of MG remains unclear.
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