Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This chronic inflammation further exacerbates adipose tissue inflammation as results of migration and activation of macrophages. Macrophages are the most abundant immune cells in the PCa microenvironment. M2 macrophages, known as Tumor-Associated Macrophages, are involved in increasing cancer malignancy. In this study, conditioned medium (TCM) of PCa cells infected with live trichomonads contained chemokines that stimulated migration of the mouse preadipocytes (3T3-L1 cells). Conditioned medium of adipocytes incubated with TCM (ATCM) contained Th2 cytokines (IL-4, IL-13). Macrophage migration was stimulated by ATCM. In macrophages treated with ATCM, expression of M2 markers increased, while M1 markers decreased. Therefore, it is suggested that ATCM induces polarization of M0 to M2 macrophages. In addition, conditioned medium from the macrophages incubated with ATCM stimulates the proliferation and invasiveness of PCa. Our findings suggest that interaction between inflamed PCa treated with T. vaginalis and adipocytes causes M2 macrophage polarization, so contributing to the progression of PCa.

Purpose: Paclitaxel is an anticancer drug that blocks cell division by stabilizing microtubules. Even though paclitaxel has been shown to be effective in killing bladder cancer cell lines in vitro, the in vivo absorption was extremely low. A paclitaxel formulation was prepared in solution only, which was bioadhesive, and its effects evaluated in the MBT-2 cell line and in C3H2 bladder cancer mice. In addition, the toxicity of the paclitaxel formulation was also evaluated. Materials and Methods: A muco-adhesive oily paclitaxel formulation was made by the combining of monoolein, tricaprylin, Tween 80 and paclitaxel. MBT-2 cells were cultivated in different concentration of taxol, and the tumoricidal activity measured by the indirect methylthiazol-2-yl-2, 5-diphenyl tetrazolium bromide (MTT) assay. In an in vivo study, the treatment regimen for the s.c. C3H2 mice was five consecutive once daily administrations, beginning on day 4 post tumor implant. The length and width of the tumors were measured twice a week, and the tumor volume calculated. On day 21, the tumor volume change and toxicity were evaluated. Results: The average particle size of paclitaxel-loaded lipid nanoparticle was about 600nm, with a polydispersity of 1,000. Only 2.6% of the MBT-2 cells were viable after 24 hour of treatment with the formulation at a paclitaxel concentration of 10mug/ml, while showing minimal toxicity of the formulation without paclitaxel. Paclitaxel-loaded lipid nanoparticles, administered orally, allowed significant antitumor activity in C3H2 mice (p<0.05). Conclusions: Paclitaxel-loaded lipid nanoparticles have a remarkable cytotoxic effect against MBT-2 cells, in a dose dependent manner, and the oral paclitaxel-loaded lipid nanoparticle therapy had an inhibitory effect on bladder tumors in a MBT-2 model, but without systemic toxicity. Therefore, oral paclitaxel-loaded lipid nanoparticles may be used for advanced bladder cancer patients.
Absorption ; Animals ; Cell Division ; Cell Line ; Homicide ; Humans ; Mice* ; Microtubules ; Nanoparticles* ; Paclitaxel ; Particle Size ; Polysorbates ; Tumor Burden ; Urinary Bladder Neoplasms* ; Urinary Bladder*

Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infected with Trichomonas vaginalis induced the proliferation of prostate cells via a leptin signaling pathway. To investigate the effect of crosstalk between adipocyte leptin and inflamed epithelial cell in proliferation of prostate cells, adipocytes 3T3-L1 cells were incubated in conditioned medium of BPH-1 cells infected with T. vaginalis (T. vaginalis-conditioned medium, TCM), and then the adipocyte-conditioned medium (ATCM) was identified to cause proliferation of prostate cells. BPH-1 cells incubated with live T. vaginalis released pro-inflammatory cytokines, and conditioned medium of these cells caused migration of adipocytes. When prostate stromal cells and BPH-1 cells were incubated with adipocyte conditioned medium containing leptin, their growth rates increased as did expression of the leptin receptor (known as OBR) and signaling molecules such as JAK2/STAT3, Notch and survivin. Moreover, blocking the OBR reduced this proliferation and the expression of leptin signaling molecules in response to ATCM. In conclusion, our findings show that inflamed BPH-1 cells infected with T. vaginalis induce the proliferation of prostate cells through leptin-OBR signaling. Therefore, it is likely that T. vaginalis contributes to prostate enlargement in BPH via adipocyte leptin released as a result of inflammation of the prostate.

Leptin is a type of adipokine mainly produced by adipocytes and reported to be overproduced in prostate cancer. However, it is not known whether it stimulates the proliferation of prostate cells. In this study, we investigated whether benign prostatic hyperplasia epithelial cells (BPH-1 cells) infected with Trichomonas vaginalis induced the proliferation of prostate cells via a leptin signaling pathway. To investigate the effect of crosstalk between adipocyte leptin and inflamed epithelial cell in proliferation of prostate cells, adipocytes 3T3-L1 cells were incubated in conditioned medium of BPH-1 cells infected with T. vaginalis (T. vaginalis-conditioned medium, TCM), and then the adipocyte-conditioned medium (ATCM) was identified to cause proliferation of prostate cells. BPH-1 cells incubated with live T. vaginalis released pro-inflammatory cytokines, and conditioned medium of these cells caused migration of adipocytes. When prostate stromal cells and BPH-1 cells were incubated with adipocyte conditioned medium containing leptin, their growth rates increased as did expression of the leptin receptor (known as OBR) and signaling molecules such as JAK2/STAT3, Notch and survivin. Moreover, blocking the OBR reduced this proliferation and the expression of leptin signaling molecules in response to ATCM. In conclusion, our findings show that inflamed BPH-1 cells infected with T. vaginalis induce the proliferation of prostate cells through leptin-OBR signaling. Therefore, it is likely that T. vaginalis contributes to prostate enlargement in BPH via adipocyte leptin released as a result of inflammation of the prostate.

The efficacy nd tolerance of topical administration of levocabastine(0.5mg/ml)were evaluated in patients with allergic conjunctivitis. A total of 166 patients who had a typical history of atopy and a positive skin test were recruited in this study. Five clinicl symptoms(itch, tearing, chemosis, lid edema and conjunctival injection) were assessed according to a four point scale before the treatment and at 1 and 2 weeks post-therapy. Total symptom severity score before the therapy, 6.68, was remarkably decreased to 2.86 at 1 week and 2.08 at 2 weeks after the treatment. The investigators rated the treatment as globally good or excellent in 68.1% of patients checked at 1 week and 72.5% at 2 weejs after treatment. And the patients evaluated that the therapy ws good to excellent in 66.9% at 1 week and 73.1% at 2 weeks after treatment. Levocabastine eye drops has a fast onet of action with 55.4% of the patients feeling symptom relief within 15 minutes after the first administration. The adverse effect was experienced in 44 patients. Ocular irritation sign, such as foreign body sensation or soreness, was the most frequently reported complaint. These results suggest that levocabastine eye drops is an effective and safe topical alternative for treatment of allergic conjunctivitis.
Administration, Topical ; Conjunctivitis, Allergic* ; Edema ; Foreign Bodies ; Humans ; Ophthalmic Solutions* ; Research Personnel ; Sensation ; Skin Tests