cholera/edema

There are indications that endolymph homeostasis is controlled by intracellular cAMP levels in cells surrounding the scala media. Cholera toxin is a potent stimulator of adenylate cyclase, i.e. it increases cAMP levels. We hypothesized that perilymphatic perfusion of cholera toxin might increase

The enzymatic activity of the three most studied bacterial toxins that increase the cytosolic cAMP level: pertussis toxin (PT), cholera toxin (CT), and anthrax edema toxin (ET), was imaged by fluorescence videomicroscopy. Three different cell lines were transfected with a fluorescence resonance

The recently introduced choleragen-induced rat foot edema model has been employed as a bioassay for evaluating the immunogenicity of three purified preparations containing cholera exo-enterotoxin antigen, choleragen, choleragenoid, and Formalin-treated choleragen (formagen). The results indicated

To evaluate a possible role for adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] and adenosine 3':5'-cyclic monophosphate in the secretion of endolymph, we studied the effect of an intra-scala media injection of purified cholera toxin (an adenylate cyclase stimulant) on cochlear

Epidemic Vibrio cholerae possess the VPI (Vibrio pathogenicity island) essential virulence gene cluster. The VPI is 41.2 kb in size and encodes 29 potential proteins, several of which have no known function. We show that the VPI-encoded Orf4 is a predicted 34-kDa periplasmic protein containing a

Anthrax edema toxin (EdTx) is an AB-type toxin that binds to anthrax toxin receptors on target cells via the binding subunit, protective Ag (PA). Edema factor, the enzymatic A subunit of EdTx, is an adenylate cyclase. We found that nasal delivery of EdTx enhanced systemic immunity to nasally

Experiments were conducted on a model of edema of albino mouse paws; a study was made of the effect of neuraminidase inhibitors on the cholerogenic effect of a filtrate of cholera vibrio culture. It appeared that addition to the filtrate of inhibitors depressed its biological activity. Since no

To induce toxicity, cholera toxin (CT) must first bind ganglioside G(M1) at the plasma membrane, enter the cell by endocytosis, and then traffic retrograde into the endoplasmic reticulum. We recently proposed that G(M1) provides the sorting motif necessary for retrograde trafficking into the

Enteropathogenic mechanisms of non-O 1 Vibrio cholerae were investigated using strains from the environment and those from fish in Toyama Prefecture. None of the 93 non-O 1 V. cholerae strains produced a detectable level of choleratoxin-like-enterotoxin (CT-like-enterotoxin) in Syncase medium, while

An antiserum specific for Vibrio cholerae exo-enterotoxin was produced by immunization of a horse with purified choleragenoid, a natural cholera toxoid. The serum has a high titer against the toxin antigen in passive hemagglutination tests and a respectable antipermeability factor activity. It also

Animal experiments suggest that the response of acute-phase proteins (APPs) modulates the inflammatory reaction following tissue injury. To study this in man we investigated the relation between a number of APPs, including fibrinogen and alpha 2-macroglobulin, and the inflammatory edema induced by a

A cholera toxoid was prepared by iodinating purified cholera toxin having an activity of 25 Limit of blueing (Lb) doses/1 microgram with 0.8 mumol of iodine monochloride per mg toxin, and the residual lesion capacity was tested in mice. The blueing dose (BD) test was strongly positive for the native

A fluid-accumulating factor (FAF in the ligated rabbit ileal loop test) from a strain of non-O1 Vibrio cholerae not producing cholera toxin-like enterotoxin (CTLT) was partially purified by ammonium sulfate precipitation, gel filtration with Sephadex G-100, and DEAE cellulose column chromatography.