Mechanism of action of Pseudomonas aeruginosa exotoxin A in experimental mouse infections: adenosine diphosphate ribosylation of elongation factor 2.

Abstract

The data presented indicate that one of the primary actions of Pseudomonas aeruginosa exotoxin during experimental infection is the inactivation of elongation factor 2 (EF-2) in various mouse organs. Organs from mice infected with the toxigenic P. aeruginosa strain PA103 contained considerably less EF-2 activity than did organs from uninfected controls. Whereas EF-2 activity was reduced in all organs examined from PA103-infected animals, the largest decrease was observed in the liver, where the active EF-2 levels were reduced by 70 to 90%. In addition, consistent inhibition of protein synthesis in livers but not in other organs was observed in mice infected with the toxigenic PA103 strain. Treatment of mice with antitoxin before infection with strain PA103 prevented inactivation of EF-2. When mice were infected with lethal doses of the nontoxigenic P. aeruginosa WR5 strain, tissue EF-2 levels were not markedly reduced below those derived from uninfected control animals.

• Authors: O R Pavlovskis, B H Iglewski, M Pollack
• Journal: Infection and immunity (Infect Immun) Vol. 19 Issue 1 Pg. 29-33 (Jan 1978) ISSN: 0019-9567 [Print] United States
• PMID: 415004 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Bacterial Toxins
• Exotoxins
• Peptide Elongation Factors
• Adenosine Diphosphate

Topics

• Adenosine Diphosphate (metabolism)
• Animals
• Bacterial Toxins (biosynthesis, pharmacology)
• Burns (metabolism)
• Disease Models, Animal
• Exotoxins (biosynthesis, pharmacology)
• Female
• Liver (metabolism)
• Mice
• Peptide Elongation Factors (analysis)
• Protein Biosynthesis
• Pseudomonas Infections (metabolism)
• Pseudomonas aeruginosa (metabolism)
• Species Specificity