Inflammatory response of a prostate stromal cell line induced by Trichomonas vaginalis.

While Trichomonas vaginalis, a cause of sexually transmitted infection, is known as a surface-dwelling protozoa, trichomonads have been detected in prostatic tissue from benign prostatic hyperplasia and prostatitis by immunoperoxidase assay or PCR. However, the immune response of prostate stromal cells infected with T. vaginalis has not been investigated. Our objective was to investigate whether T. vaginalis could induce an inflammatory response in prostate stromal cells. Incubation of a human prostate stromal myofibroblast cells (WPMY-1) with live T. vaginalis T016 increased expression of the inflammatory chemokines CXCL8 and CCL2. In addition, TLR4, ROS, MAPK and NF-κB expression increased, while inhibitors of TLR4, ROS, MAPKs and NF-κB reduced CXCL8 and CCL2 production. Medium conditioned by incubation of WPMY-1 cells with T. vaginalis stimulated the migration of human neutrophils and monocytes (THP-1 cells). We conclude that T. vaginalis increases CXCL8 and CCL2 production by human prostate stromal cells by activating TLR4, ROS, MAPKs and NF-κB, and this in turn attracts neutrophils and monocytes and leads to an inflammatory response. This study is the first attempt to demonstrate an inflammatory reaction in prostate stromal cells caused by T. vaginalis.

Histamine and TNF-alpha release by rat peritoneal mast cells stimulated with Trichomonas vaginalis.

Mast cells have been reported to be predominant in the vaginal smears of patients infected with T. vaginalis. In this study, we investigated whether T. vaginalis could induce mast cells to migrate and to produce TNF-alpha and histamine. Rat peritoneal mast cells (RPMC), a primary mast cell, were used for the study. T. vaginalis induced an increase in chemotactic migration of the mast cells toward excretory and secretory product (ESP) of T. vaginalis, and the mast cells activated with T. vaginalis showed an increased release of histamine and TNF-alpha. Therefore, mast cells may be involved in the inflammatory response caused by T. vaginalis.

Correlation of antiviral T-cell responses with suppression of viral rebound in chronic hepatitis B carriers: a proof-of-concept study.

Despite recent advances in the chemotherapy of chronic hepatitis B (CHB), an effective viral suppression after cessation of therapy has not yet been achieved. To investigate whether hepatitis B virus (HBV)-specific T-cell responses are inducible and can contribute to the viral suppression after cessation of the therapy, we conducted a proof-of-concept study with a DNA vaccine comprising of most HBV genes plus genetically engineered interleukin-12 DNA (IL-12N222L) in 12 CHB carriers being treated with lamivudine (LAM). When the ex vivo and/or cultured IFN-gamma enzyme-linked immunospot (ELISPOT) assay was performed, the detectable HBV-specific IFN-gamma secreting T-cell responses were observed at the end of treatment and during a follow-up. These type 1T-cell responses, particularly CD4(+) memory T-cell responses could be maintained for at least 40 weeks after the therapy and correlated with virological responses, but not with alanine aminotransferase elevation. Moreover, DNA vaccination under LAM treatment appeared to be well-tolerated and showed 50% of virological response rate in CHB carriers. Thus, a combination therapy of the DNA vaccine with chemotherapy may be one of new immunotherapeutic methods for the cure of CHB.

Effects of the aqueous extract of epimedii herba on the antibody responses in mice.

Antibodies and cytokines in serum were detected in male ICR mice treated with the aqueous extract of Epimedii Herba (AEEH) at doses of 40, 120 and 360 mg/kg orally for 2 weeks. Effects of AEEH on antibody forming responses were assessed by enzyme linked immunosorbent assay (ELISA) of immunoglobulin (Ig) levels in serum collected 7 days after priming with ovalbumin (OVA) in complete Freund's adjuvant (CFA) or immediately without priming at week 2. The relative spleen weight was significantly increased by AEEH, compared with controls, especially at a dose of 120 mg/kg of it after priming with OVA and 40 mg/kg without priming, respectively. However, body weight gain was slightly decreased in AEEH-fed mice. The enhancement of total serum IgG and IgG1 levels in unprimed mice was statistically significant in mice fed 40 mg/kg AEEH. Total serum IgG2a levels and Il-4 secretion were also statistically augmented by all groups of AEEH treatment. A tendency to marked increase of total serum IgM level and IFN-gamma secretion was also observed in mice fed 40 and 120 mg/kg AEEH but not those fed 360 mg/kg AEEH. When mice were immunized with OVA, furthermore, a marked stimulation of antibody formation and cytokines secretion was observed in all groups of AEEH-fed mice compared with controls. These findings indicate that AEEH at therapeutic concentrations enhances the production of antibodies and cytokines in mice, and the enhancing effects are more marked when the mice were immunized with OVA. Thus, these results suggest that AEEH is effective on Th cell functions, and protective effects on host against immune diseases.