Abstract
Pseudomonas aeruginosa, as an opportunistic pathogen, establishes a chronic infection in the respiratory track of patients suffering from pneumonia and bronchiectasis, including cystic fibrosis. Biofilm formation inside the oversecreted mucus layer lining the patient airway and production of virulence factors, a process controlled by quorum sensing, are considered to be the major virulence determinants in P. aeruginosa pathogenesis. Recently, an abnormally thickened mucus layer was proven to be anaerobic. Given the fact that currently used antibiotics are less effective under anaerobic environments, these new findings lead us to change the way we confront P. aeruginosa infection. This article reviews pathological features of patient airways that become susceptible to P. aeruginosa infection and bacterial adaptation that contributes to the prolonged survival inside the patient airway.
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Figure 1.
Schematic comparison between normal (A) and diseased (B) airway mucus environments. Maintenance of periciliary liquid layer (PLL) with constant depth and appropriate movement of the mucus layer on top of the PLL, which mediates the mucociliary clearance, is achieved in normal airways. In diseased states, however, PLL is depleted and an abnormally oversecreted (and thus, highly viscous) mucus layer is formed. This mucus layer is highly susceptible to bacterial colonization.
![jbv-40-59f1.tif](/upload/SynapseXML/0079jbv/thumb/jbv-40-59f1.gif)
Figure 2.
Aerobic (A) vs. anaerobic (B) respiratory pathways in P. aeruginosa. P. aeruginosa can use either oxygen or nitrate/nitrite as electron acceptors in the electron transport chain. NADH DH, NADH dehydrogenase; Cyt bc1, cytochrome bc1 complex; Cyt oxidase, cytochrome oxidase; NAR, nitrate (NO3–) reductase; NIR, nitrite (NO2–) reductase; NOR, nitric oxide reductase; N2OR, nitrous oxide (N2O) reductase.
![jbv-40-59f2.tif](/upload/SynapseXML/0079jbv/thumb/jbv-40-59f2.gif)