Clinical Trial: Role of Toxins in Lung Infections Caused by Pseudomonas Aeruginosa

Study Status: Recruiting
Recruit Status: Recruiting
Study Type: Observational

Official Title: Role of Exotoxins in the Pathogenesis of Pseudomonas Aeruginosa

Brief Summary:

Some bacteria that cause disease can produce toxic substances that may worsen the disease. Pseudomonas aeruginosa is a bacteria that can produce a variety of toxins and is of special interest for patients with cystic fibrosis and repeated long term lung infections.

The goal of this study is to determine whether specific toxins produced by Pseudomonas aeruginosa may be important in the disease process of chronic lung infections of patients with cystic fibrosis.

This study will attempt to measure bacterial production of toxins in blood and sputum and immune system response to toxins in the blood.

Detailed Summary: The goal of this study is to determine whether virulence determinants that use the type III-secretory pathway may be important in the pathogenesis of chronic Pseudomonas aeruginosa lung infections in patients with cystic fibrosis (CF). The studies will quantify bacterial effector proteins in serum and sputum and the immune response to specific products as reflected by antibodies in serum. Candidate effector proteins include: (1) exotoxin A, a non-type III-dependent ADP-ribosyltransferase and cytotoxin that does not use the Type III secretory pathway, (2) ExoS, a type III pathway-dependent extracellular ADP-ribosyltransferase with cytotoxic activity, (3) ExoU, another type III-dependent cytotoxin, that is responsible for epithelial injury in acute lung infections, and (4) PcrV, a homolog to the V antigen of Yersinia.
Sponsor: National Heart, Lung, and Blood Institute (NHLBI)

Current Primary Outcome:

Original Primary Outcome:

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Original Secondary Outcome:

Information By: National Institutes of Health Clinical Center (CC)

Dates:
Date Received: November 27, 2001
Date Started: February 4, 1998
Date Completion:
Last Updated: April 20, 2017
Last Verified: March 2, 2017