Differential response of Vibrio cholerae planktonic and biofilm cells to autoinducer 2 deficiency

The formation of biofilm communities enhances the persistence of Vibrio cholerae in aquatic environments. Biofilm production is repressed by the quorum-sensing regulator HapR in response to the accumulation of CAI-1 and AI-2. CAI-1 is the strongest input signal activating HapR, whereas the role of AI-2 remains ill-defined. In the present study, we show that a V. cholerae luxS (AI-2-defective) mutant made increased biofilm. Interestingly, cells in the biofilm were more responsive to AI-2 deficiency than cells from the planktonic population.     

Overexpression of a Mutant B Subunit in Toxigenic Vibrio cholerae Diminishes Production of Active Cholera Toxin In Vivo

A mutant cholera toxin B subunit containing a G33E substitution was constructed and expressed in V. cholerae. The G33E amino acid substitution did not affect the amount of recombinant CTB secreted to the culture medium. The overexpression of the mutant B subunits in wild-type toxigenic cholera vibrios led to an 80% decrease in production of active cholera toxin in vitro and in vivo. Overexpression of B^G33E subunits could be instrumental in the increase of the biosafety of live attenuated cholera candidate vaccine strains. Received: 29 January 1998 / Accepted: 30 April 1998     

Effect of streptozotocin-diabetes and insulin treatment on regulation of Leydig cell function in the rat

The present study was performed to further clarify the possible role played by insulin deficiency on the steroidogenic capacity of the rat testis. Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by i.p. injection (40 mg/kg b.w.) of streptozotocin and was monitored at 2-day intervals by measuring body weight and serum glucose, glucosuria and ketonuria levels. The effect of insulin therapy on pituitary LH content and plasma LH concentrations, as well as on the cyclic AMP level in interstitial cell incubation medium and plasma testosterone concentrations, was measured 30 days after the induction of diabetes by radioimmunoassay. Streptozotocin-induced diabetes resulted in significantly reduced pituitary LH (16%, P less than 0.025) and plasma LH (34%, P less than 0.02); insulin treatment completely restored these levels. Similarly, the cyclic AMP content of interstitial cell incubation medium and the plasma testosterone concentrations were dramatically decreased in the diabetic state (50%, P less than 0.005 and 63%, P less than 0.025, respectively) and combined treatment with insulin plus hCG appeared slightly more effective than treatment with either of these hormones alone, suggesting a possible synergistic action. It is concluded that decreased testicular steroidogenesis in the diabetic rat may represent, at least in part, a direct consequence of insulin deficiency at the hypothalamic and/or pituitary levels. However, our findings would also be consistent with other reports suggesting that insulin may play a direct role in the rat testis.