ABSTRACT
Abstract The goal of this review is to highlight new developments that could lead to better treatment strategies for complications associated with chronic Pseudomonas aeruginosa infections in cystic fibrosis (CF) airway disease. Recent data suggest that P. aeruginosa grows anaerobically in “biofilms” enmeshed in the thick airway mucus of CF patients. The most energy-efficient form of anaerobic growth by P aeruginosa is via respiration using nitrate (N 0 3 ) or nitrite (N 02 ) as a terminal electron acceptor. Both of these nitrogen oxides are amply present in CF airway surface liquid. In this review, we discuss how the anaerobic biofilm mode of growth actually benefits P. aeruginosa in the context of CF airway disease. We will also describe in detail the anaerobic respiratory pathway and how enzymatic production and disposal of a gaseous by-product of anaerobic growth, nitric oxide (NO), is tightly regulated and critical for anaerobic survival during respiration. We next describe how the process of intercellular communication known as quorum sensing is necessary for anaerobic survival of P. aeruginosa. Finally, when P. aeruginosa shifts to a mucoid, alginate-overproducing form, the anaerobic biofilm mode of growth and anaerobic metabolism is further promoted. Thus, it is our belief that new therapeutic strategies aimed at targeting anaerobic gene products and determining the effectiveness of various anti-P. aeruginosa antibiotics under anaerobic conditions need to be developed to help combat these infections.
