Distribution of Toxin Genes and Enterotoxins in Bacillus thuringiensis Isolated from Microbial Insecticide Products.

Bacillus thuringiensis microbial insecticide products have been applied worldwide. Although a few cases of B. thuringiensis foodborne illness have been reported, little is known about the toxigenic properties of B. thuringiensis isolates. The aims of this study were to estimate the pathogenic potential of B. thuringiensis selected from microbial insecticide products, based on its possession of toxin genes and production of enterotoxins. Fifty-two B. thuringiensis strains selected from four kinds of microbial insecticide products were analyzed. PCR assay for detection of toxin genes and immunoassay for detection of enterotoxins were performed. The hemolysin BL complex as a major enterotoxin was produced by 17 (32.7%), whereas the nonhemolytic enterotoxin complex was detected in 1 (1.9%) of 52 B. thuringiensis strains. However, cytK, entFM, and ces genes were not detected in any of the tested B. thuringiensis strains. The potential risk of food poisoning by B. thuringiensis along with concerns over B. thuringiensis microbial insecticide products has gained attention recently. Thus, microbial insecticide products based on B. thuringiensis should be carefully controlled.

Over-expression of thymosin ß4 in granulomatous lung tissue with active pulmonary tuberculosis.

Recent studies have shown that thymosin ß4 (Tß4) stimulates angiogenesis by inducing vascular endothelial growth factor (VEGF) expression and stabilizing hypoxia inducible factor-1α (HIF-1α) protein. Pulmonary tuberculosis (TB), a type of granulomatous disease, is accompanied by intense angiogenesis and VEGF levels have been reported to be elevated in serum or tissue inflamed by pulmonary tuberculosis. We investigated the expression of Tß4 in granulomatous lung tissues at various stages of active pulmonary tuberculosis, and we also examined the expression patterns of VEGF and HIF-1α to compare their Tß4 expression patterns in patients' tissues and in the tissue microarray of TB patients. Tß4 was highly expressed in both granulomas and surrounding lymphocytes in nascent granulomatous lung tissue, but was expressed only surrounding tissues of necrotic or caseous necrotic regions. The expression pattern of HIF-1α was similar to that of Tß4. VEGF was expressed in both granulomas and blood vessels surrounding granulomas. The expression pattern of VEGF co-localized with CD31 (platelet endothelial cell adhesion molecule, PECAM-1), a blood endothelial cell marker, and partially co-localized with Tß4. However, the expression of Tß4 did not co-localize with alveolar macrophages. Stained alveolar macrophages were present surrounding regions of granuloma highly expressing Tß4. We also analyzed mRNA expression in the sputum of 10 normal and 19 pulmonary TB patients. Expression of Tß4 was significantly higher in patients with pulmonary tuberculosis than in normal controls. These data suggest that Tß4 is highly expressed in granulomatous lung tissue with active pulmonary TB and is associated with HIF-1α- and VEGF-mediated inflammation and angiogenesis. Furthermore, the expression of Tß4 in the sputum of pulmonary tuberculosis patients can be used as a potential marker for diagnosis.

Possible role of ginsenoside Rb1 on regulation of rat liver triglycerides.

We have studied the effects of ginsenoside Rb1 (GRb1) on the change in lipid contents in rat liver. When GRb1 was administered intraperitoneally to rats, liver microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity were lower than those in control rats. The contents of triglyceride (TG) and cholesterol were decreased, but those of total phospholipid, phosphatidylcholine, and phosphatidylethanolamine were increased in the GRb1-treated group compared with controls. These results indicate that GRb1 might be involved in lipid metabolism by regulating the activity of microsomal cytochrome P-450 monooxygenase. Although liver TG levels were reduced by GRb1, the levels of TG and beta-lipoprotein in serum from the GRb1-treated group did not change as compared with those in controls. Thus we suggest that the decrease in liver TG levels with GRb1-treatment is not associated with the secretion of TG-rich very low-density lipoprotein. Furthermore, the level of cAMP was also significantly increased in the GRb1-treated group as compared with that in controls. Additionally, the cAMP level was more markedly increased as compared with that in the GRb1-treated group or control group when GRb, was exogenously added to the reaction system for measuring cAMP production in homogenates from control group liver. Accordingly, these results demonstrate that GRb1 might lower TG levels via cAMP-production in the liver, and GRb1 might be an interesting candidate to for a modulator of cAMP-mediated effects, especially within the liver steatosis system.