Kolaviron shows anti-proliferative effect and down regulation of vascular endothelial growth factor-C and toll like receptor-2 in Wuchereria bancrofti infected blood lymphocytes.

The anti-proliferative effect and down regulation of vascular endothelial growth factor C and toll like receptor-2 by kolaviron on Wuchereria bancrofti infected peripheral blood lymphocytes were investigated. Blood were collected from consenting volunteers in Talata Mafara, Nigeria, between the hours of 10pm to 12am, and microscopically identified for microfilariae. W. bancrofti positive samples were cultured for 72h treated with Doxycycline (2µg/ml) and kolaviron (5µg/ml) in vitro. Mitotic index, expression of vascular endothelial growth factor-C (VEGF-c), toll like receptor-2 (TLR-2) were determined using standard procedures. Mitotic index was significantly (P<0.05) reduced in the kolaviron treated group compared to negative control. Kolaviron also significantly (P<0.05) down regulated the expression of VEGF-c and TLR-2 when compared with the untreated group. In both cases, the effects of kolaviron was not significantly different (P<0.05) to that of doxycycline. Furthermore, strong positive correlations between mitotic index, VEGF-c and TLR-2 expressions were observed. The study suggests that kolaviron rich portion of Garcinia kola exhibited anti-proliferative effect and down regulation of VEGF-c and TLR-2 in W. bancrofti infected blood. Thus, the results from this study might have unravelled the potency of kolaviron in the management of complications associated with lymphatic filariasis.

Pathogenic mechanisms of Trypanosoma evansi infections.

Insect-borne diseases exact a high public health burden and have a devastating impact on livestock and agriculture. To date, control has proved to be exceedingly difficult. One such disease that has plagued sub-Saharan Africa is caused by the protozoan African trypanosomes (Trypanosoma species) and transmitted by tsetse flies (Diptera: Glossinidae). This presentation describes Trypanosoma evansi (T. evansi) which causes the disease known as trypanosomosis (Surra) or trypanosomiasis in which several attempts have being made to unravel the clinical pathogenic mechanisms in T. evansi infections, yielding various reports which have implicated hemolysis associated to decrease in life span of erythrocytes and extensive erythrophagocytosis being among those that enjoy prominence. T. evansi generates Adenosine Triphosphate (ATP) from glucose catabolism which is required for the parasite motility and survival. Oxidation of the erythrocytes induces oxidative stress due to free radical generation. Lipid peroxidation of the erythrocytes causes membrane injury, osmotic fragility and destruction of the red blood cell (RBC) making anemia a hallmark of the pathology of T. evansi infections.