Clostridium perfringens alpha toxin affects electrophysiological properties of isolated jejunal mucosa of laying hens.
Bacteria that colonize the intestinal tract can invade epithelial cells or produce toxins that cause diarrhoeal diseases. Proliferation of Clostridium perfringens and production of alpha-toxin, a phospholipase C, is the major factor for necrotic enteritis in poultry. However, little is known about the functional importance of luminal alpha-toxin during intestinal infection. The purpose of this study was to investigate the effects of purified alpha toxin of Clostridium perfringens on the electrophysiology of the laying hen's stripped jejunum in Ussing chambers. The effects were investigated in Experiment 1 after toxin addition to the mucosal and serosal side of the tissue, and a second experiment was performed to study the effect of the toxin on sodium-dependent glucose transport. Mucosal exposure of jejunal tissue sheets to 100 units of alpha toxin/L did not elicit electrophysiologic changes. The addition of purified alpha toxin to the serosal side induced a biphasic increase in short-circuit current (ISC) after 15 and 100 min. The magnitude of the increase of ISC of both peaks was similar, but the second phase response lasted longer. The tissue conductivity tended (P = 0.07) to be lower after 2 h of toxin addition compared with basal value when no toxin was added. In the second experiment, adding D-glucose on the mucosal side of the jejunum increased (P < 0.05) the ISC from a baseline value of 42 +/- 28 microA/cm2 to a maximal value of 103 +/- 27 microA/cm2. Preincubation with alpha-toxin almost fully inhibited this stimulation of ISC by D-glucose. The conductance of the tissues was not affected by the toxin addition. These findings indicate that alpha toxin not only causes electrogenic secretion of anions, probably due to the stimulation of chloride secretion, but also diminishes electrogenic Na+/glucose cotransport from the mucosal to serosal side in the small intestine of poultry.
Rehman
H
H
Institute of Nutrition, Department of Veterinary Public Health and Food Science, University of Veterinary Medicine, Vienna, Austria.
Awad
W A
WA
Lindner
I
I
Hess
M
M
Zentek
J
J
D000818:Animals; D001427:Bacterial Toxins / Q000494:pharmacology*; D002135:Calcium-Binding Proteins / Q000494:pharmacology*; D002645:Chickens / Q000502:physiology*; D004594:Electrophysiology; D005260:Female; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism*; D007583:Jejunum / Q000166:cytology*; D010738:Type C Phospholipases / Q000494:pharmacology*
D001427:Bacterial Toxins; D002135:Calcium-Binding Proteins; D010738:Type C Phospholipases; C040649:alpha toxin, Clostridium perfringens