trehalose-6-6--dibehenate and Disease-Models--Animal

Topics: Adjuvants, Immunologic; Animals; CD4-Positive T-Lymphocytes; Cytokines; Disease Models, Animal; Drug Compounding; Female; Glycolipids; Host-Pathogen Interactions; Immunogenicity, Vaccine; Lipid A; Liposomes; Lung; Mice, Inbred C57BL; Mycobacterium tuberculosis; Quaternary Ammonium Compounds; Receptors, Pattern Recognition; Time Factors; Tuberculosis Vaccines; Tuberculosis, Pulmonary; Vaccination; Vaccines, Subunit; Virulence

To investigate the effect of PKC δ gene on the anti-tuberculosis activity of macrophages and the mechanism.. Bone marrow cells of PKC δ knockout mice and wild-type mice were cultured and L929 cells were induced to differentiate into macrophages. Lipopolysaccharide (LPS) and trehalose 6,6'-dimycolate (TDM) were used to stimulate macrophages respectively. After 24 and 96 hours, cells and the supernatant were collected to evaluate the inflammatory cytokines produced by macrophages using ELISA method. Real-time PCR was performed to detect the expression of macrophage mRNA level and nitric oxide (NO) production of macrophages was measured by NO assay.. The results showed that, after TDB stimulation, IL-1β, IL-6, and other cytokines, as well as NO produced by macrophages of PKC δ knockout mice, were significantly decreased (p < 0.01) compared with the wild-type mice. In PKC δ knockout macrophages, the above protein-coding genes were also decreased significantly at the transcriptional level (p < 0.01).. PKC δ can enhance the anti-tuberculosis capacity of macrophages by inducing to the release of inflammatory factors by macrophages.

Topics: Animals; Cell Line; Disease Models, Animal; Glycolipids; Humans; Inflammation Mediators; Lipopolysaccharides; Macrophages; Mice; Mice, Knockout; Mycobacterium tuberculosis; Primary Cell Culture; Protein Kinase C-delta; Tuberculosis