sq-23377 and Cysticercosis

Annexin B1 is a novel member of the annexin superfamily which was isolated from a Cysticercus cellulosae cDNA library. To investigate the physiological roles of annexin B1, we firstly performed immunohistochemical analysis on frozen Cysticercus cellulosae sections and found that annexin B1 was present not only in the tegument of the bladder wall, but also in the host-derived inflammatory layer; In addition, ELISA analysis revealed that annexin B1 could be detected in the cystic fluid of Cysticercus cellulosae and the sera of pigs with cysticercosis. These findings indicated that annexin B1 might be a secretary protein. We further constructed a pEGFP-annexin B1 plasmid and transfected it into SiHa cells. We found that GFP-annexin B1 was stimulated to translocate to the plasma membrane by phorbol 12-myristate 13-acetate (PMA). By contrast, it was induced to distribute at the plasma and nuclear membranes by treatment with calcium ionophore ionomycin. PMA increased annexin B1 membrane binding, which might facilitate exocytosis. Moreover, translocation of the protein to the plasma and nuclear membranes after stimulated by ionomycin, was predicted to be related to an additional function.

Topics: Animals; Annexins; Calcium; Cysticercosis; Cytosol; Female; Helminth Proteins; Humans; Immunohistochemistry; Ionomycin; Phorbol Esters; Swine; Taenia solium; Tumor Cells, Cultured; Uterine Cervical Neoplasms

Infection of intermediate hosts with eggs of taeniid parasites results in a larval infestation known as cysticercosis. A number of studies have indicated that cysticercosis is associated with immunosuppression, although little is known about the mechanisms involved. In the present study, mice infected with the larvae of Taenia crassiceps were found to exhibit a pronounced energy, which preferentially affected T-cells located anatomically close to the parasite. This anergy was linked to late events in the T cell activation pathway; that is, stimulation through the T cell receptor(TCR)/CD3 complex by Concanavalin-A, or plate-bound monoclonal antibodies (mAb) to TCR alpha beta or CD3 epsilon, or combinations of phorbol ester and ionomycin (all of which can bypass early membrane-related events), failed to fully activate T lymphocytes. The relative proximity of T cells to the parasite was directly related to upregulation of IL-4 and downregulation of IL-2 production. In addition, the profiles of parasite-specific Abs showed an exclusive increase of serum IgG1 during infection. Taken together, the data suggest that infection of mice with larvae of T. crassiceps alters the balance of CD4+ Th cells by upregulating Th2 and downregulating Th1 cells located in close proximity to the parasite.

Topics: Animals; Antibodies, Helminth; CD3 Complex; Clonal Anergy; Cysticercosis; Down-Regulation; Female; Immunoglobulin Isotypes; Interleukin-2; Interleukin-4; Ionomycin; Ionophores; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Protein Kinase C; Receptors, Antigen, T-Cell, alpha-beta; Signal Transduction; Spleen; Tetradecanoylphorbol Acetate; Th1 Cells; Th2 Cells