Format

Send to:

Choose Destination
See comment in PubMed Commons below
Microb Pathog. 2005 Feb-Mar;38(2-3):133-7.

'In vivo' studies on the pathophysiological mechanism of Vibrio parahaemolyticus TDH(+)-induced secretion.

Author information

  • 1Istituto di Scienze Tossicologiche, Igienistiche ed Ambientali, University of Urbino, via S. Chiara 27, 61029 Urbino, Italy. baffone@uniurb.it

Abstract

The thermostable direct haemolysin (TDH) is considered to be the major virulence factors of Vibrio parahaemolyticus; however, poor information is available about its mechanism of action. In our study we examined the capacity of two V. parahaemolyticus TDH-producers (strains 2067 and 3305) to induce fluid secretion in rat ileal loop and to reveal the role of calcium ions (Ca(2+)), calmodulin (CaM), and protein kinase C (PKC) in V. parahaemolyticus TDH(+)-induced fluid secretion. The results show that V. parahaemolyticus TDH(+) strains were able to induce secretion in small intestine; on the contrary, this ability was not evidenced in the V. parahaemolyticus TDH(-) strain used as negative control. The data suggest an enterotoxic activity of haemolysin. Calcium ionophore A23187 and 1-verapamil (calcium channel blocker), when injected alone, induced fluid accumulation in the control loops. A further increase in fluid accumulation (P<0.001) was noted when calcium ionophore was injected along with bacterial suspension of both TDH(+) strains and a significant decrease (P<0.001) in experimental loops when 1-verapamil was inoculated along with bacterial suspension. The other modulating agents increased fluid accumulation in both control and experimental loops, without significant differences with respect to the positive control. Our findings suggest that Ca(2+) appears to be an important messenger involved in the stimulation of intestinal secretion, contrary to PKC and calmodulin which do not appear to have any role.

PMID:
15748815
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk