title: Positive correlation of algD transcription to lasB and lasA transcription by populations of Pseudomonas aeruginosa in the lungs of patients with cystic fibrosis.
abstract: Pseudomonas aeruginosa causes a chronic infection in the lungs of individuals with cystic fibrosis. The P. aeruginosa isolates from these infections, when grown under laboratory conditions, characteristically are mucoid and produce low levels of the more destructive virulence factors, such as exotoxin A and the proteases. We wanted to determine if during the chronic lung infections associated with CF, the expression of alginate was inversely correlated to the expression of exotoxin A, elastase, and the LasA protease. We measured the transcript accumulation of algD, a marker of alginate, toxA, the structural gene for exotoxin A, lasB, the structural gene for elastase, and lasA, the structural gene for LasA protease, from the sputum bacterial populations of 23 patients. In the 131 samples tested, we frequently detected transcripts from the four genes. When a Spearman rank correlation analysis was done on the samples, we found no correlation between algD transcript accumulation and toxA transcript accumulation. This result suggested that toxA was regulated independently of algD. Curiously, we found a positive correlation between algD transcript accumulation and both lasB and lasA transcript accumulation levels. This correlation may not indicate a direct association between algD and either lasA or lasB. More likely, it indicates a common regulatory element in a cascade of regulators or a common environmental cue that triggers transcription.
authors.affiliation: Department of Biological Sciences, University of Calgary, Alberta, Canada. storey@acs.ucalgary.ca
authors.forename: D G
authors.initials: DG
authors.lastname: Storey
authors.forename: E E
authors.initials: EE
authors.lastname: Ujack
authors.forename: I
authors.initials: I
authors.lastname: Mitchell
authors.forename: H R
authors.initials: HR
authors.lastname: Rabin
mesh_terms: D036002:ADP Ribose Transferases; D000293:Adolescent; D000328:Adult; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D002237:Carbohydrate Dehydrogenases / Q000096:biosynthesis; D002648:Child; D003550:Cystic Fibrosis / Q000150:complications / Q000382:microbiology*; D005098:Exotoxins / Q000096:biosynthesis; D005260:Female; D015964:Gene Expression Regulation, Bacterial; D005798:Genes, Bacterial; D014644:Genetic Variation; D006801:Humans; D008171:Lung Diseases / Q000150:complications / Q000382:microbiology*; D008297:Male; D008666:Metalloendopeptidases / Q000096:biosynthesis; D011552:Pseudomonas Infections / Q000150:complications / Q000382:microbiology*; D012329:RNA, Bacterial / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D013183:Sputum / Q000382:microbiology; D014158:Transcription, Genetic; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A
chemical_list: D036002:ADP Ribose Transferases; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D002237:Carbohydrate Dehydrogenases; D005098:Exotoxins; D008666:Metalloendopeptidases; D012329:RNA, Bacterial; D012333:RNA, Messenger; D037521:Virulence Factors; D000097668:Pseudomonas aeruginosa Exotoxin A; C020562:GDPmannose dehydrogenase; C043859:pseudolysin, Pseudomonas aeruginosa; C066371:staphylolytic protease