POSITIVE CORRELATION OF ALGD TRANSCRIPTION TO LASB AND LASA TRANSCRIPTION BY POPULATIONS OF PSEUDOMONAS-AERUGINOSA IN THE LUNGS OF PATIENTSWITH CYSTIC-FIBROSIS

Citation
Dg. Storey et al., POSITIVE CORRELATION OF ALGD TRANSCRIPTION TO LASB AND LASA TRANSCRIPTION BY POPULATIONS OF PSEUDOMONAS-AERUGINOSA IN THE LUNGS OF PATIENTSWITH CYSTIC-FIBROSIS, Infection and immunity, 65(10), 1997, pp. 4061-4067
Citations number
71
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
65
Issue
10
Year of publication
1997
Pages
4061 - 4067
Database
ISI
SICI code
0019-9567(1997)65:10<4061:PCOATT>2.0.ZU;2-4
Abstract
Pseudomonas aeruginosa causes a chronic infection in the lungs of indi viduals,vith cystic fibrosis. The P. aeruginosa isolates from these in fections, when grown under laboratory conditions, characteristically a re mucoid and produce low levels of the more destructive virulence fac tors, 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 accumulati on of algD, a marker of alginate, toxA, the structural gene for exotox in A, lasB, the structural gene for elastase, and lasA, the structural gene for LasA protease, from the sputum bacterial populations of 23 p atients. In the 131 samples tested, we frequently detected transcripts from the four genes. When a Spearman rank correlation analysis was do ne on the samples, we found no correlation between algD transcript acc umulation and toxA transcript accumulation. This result suggested that toxA,vas regulated independently of algD. Curiously, we found a posit ive correlation between algD transcript accumulation and both lasB and lasA transcript accumulation levels. This correlation may not indicat e a direct association between algD and either lasA or lasB. More like ly, it indicates a common regulatory element in a cascade of regulator s or a common environmental cue that triggers transcription.