1 Disciplines of Medicine, University of Tasmania Clinical School, 43 Collins Street, Hobart, Tasmania, 7000, Australia
2 Disciplines of Pathology, University of Tasmania Clinical School, 43 Collins Street, Hobart, Tasmania, 7000, Australia
Correspondence
David W. Reid
(d.e.c.reid{at}utas.edu.au)
We read with interest the article by Kim et al. (2003), but disagree with the conclusion that their in vitro culture conditions are similar to those encountered by Pseudomonas aeruginosa in the cystic fibrosis (CF) lung. Contrary to current dogma, we have previously shown that the CF lung is not iron deplete but rather that the opposite situation exists! (Reid et al., 2002
). There are other data to support these findings (Reid et al., 2002
; Stites et al., 1998
, 1999
). Furthermore, as well as living in an environment rich in iron, it has recently been established that P. aeruginosa exists in the CF lung in anaerobic biofilms (Costerton, 2002
). The explanation for, and consequences of, the high iron content in the CF lung is the focus of our current research but we would strongly recommend that future investigations into hostmicrobial interactions are based on accurate knowledge of the true micro-environment encountered in CF. Whether the anaerobic existence adopted by P. aeruginosa in the CF airway is actually a direct consequence of the iron-replete environment is a fascinating question, but the data of Kim et al. (2003)
do strongly suggest this may be one potential explanation. Finally, our preliminary experiments have consistently shown that clinical isolates of P. aeruginosa from CF patients are far less efficient at forming biofilms in standard tube and plate laboratory assays than the laboratory strain PAO1. Interestingly, the response of clinical isolates to alterations in environmental iron is also different to PAO1. These observations suggest phenotypic differences between these various organisms but we would argue that PAO1 is not the ideal organism to study if we are to make clinically relevant comments on the role of P. aeruginosa in CF lung disease, particularly with respect to iron and biofilms.
REFERENCES
Costerton, J. W. (2002). Anaerobic biofilm infections in cystic fibrosis. Mol Cell 10, 699700.[Medline]
Kim, E. J., Sabra, W. & Zeng, A. P. (2003). Iron deficiency leads to inhibition of oxygen transfer and enhanced formation of virulence factors in cultures of Pseudomonas aeruginosa PAO1. Microbiology 149, 26272634.
Reid, D. W., Withers, N. J., Francis, L., Wilson, J. W. & Kotsimbos, T. C. (2002). Iron deficiency in cystic fibrosis: relationship to lung disease severity and chronic Pseudomonas aeruginosa infection. Chest 121, 4854.
Stites, S. W., Walters, B., O'Brien-Ladner, A. R., Bailey, K. & Wesselius, L. J. (1998). Increased iron and ferritin content of sputum from patients with cystic fibrosis or chronic bronchitis. Chest 114, 814819.
Stites, S. W., Plautz, M. W., Bailey, K., O'Brien-Ladner, A. R. & Wesselius, L. J. (1999). Increased concentrations of iron and isoferritins in the lower respiratory tract of patients with stable cystic fibrosis. Am J Respir Crit Care Med 160, 796801.
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