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Review
. 2005 Jun 1;171(11):1209-23.
doi: 10.1164/rccm.200408-1044SO. Epub 2005 Feb 1.

Pathogen-host interactions in Pseudomonas aeruginosa pneumonia

Ruxana T Sadikot  1 , Timothy S Blackwell, John W Christman, Alice S Prince
Affiliations
Review

Pathogen-host interactions in Pseudomonas aeruginosa pneumonia

Ruxana T Sadikot et al. Am J Respir Crit Care Med. .

Abstract

Pseudomonas aeruginosa is an important pathogen causing a wide range of acute and chronic infections. P. aeruginosa rarely causes infection in the normal host, but is an efficient opportunistic pathogen causing serious infections in patients who are mechanically ventilated, individuals who are immunocompromised, and patients with malignancies or HIV infection. Among these risk groups, the most vulnerable hosts are neutropenic and patients who are mechanically ventilated. In addition, P. aeruginosa is the most prevalent chronic infection contributing to the pathogenesis of cystic fibrosis. Because of the ubiquitous nature of P. aeruginosa and its ability to develop resistance to antibiotics, it continues to be problematic from a treatment perspective. The pathogenicity of P. aeruginosa is largely caused by multiple bacterial virulence factors and genetic flexibility enabling it to survive in varied environments. Lung injury associated with P. aeruginosa infection results from both the direct destructive effects of the organism on the lung parenchyma and exuberant host immune responses. This article focuses on the major bacterial virulence factors and important aspects of the host immunity that are involved in the pathogenesis of serious P. aeruginosa infection. In addition to antibiotic therapy, strategies directed toward enhancing host defense and/or limiting excessive inflammation could be important to improve outcome in P. aeruginosa lung infections.

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Figures

<b>Figure 1.</b>
Figure 1.
Histopathology of infected cystic fibrosis (CF) airways. A hematoxylin–eosin-stained section of CF lung tissue at the time of lung transplantation is shown. Note that, despite accumulation of polymorphonuclear neutrophils (PMNs), mucin, and bacteria in the airway, the epithelial tight junctions appear intact. Bacteria are enmeshed in mucin not juxtaposed to the airway surface or within cells. (Courtesy of Michael Welsh, University of Iowa.)
<b>Figure 2.</b>
Figure 2.
Electron photomicrograph of Pseudomonas aeruginosa microcolonies in CF sputum. (Courtesy of Pradeep Singh, University of Iowa.)
<b>Figure 3.</b>
Figure 3.
A representative image of P. aeruginosa with its virulence factors: surface factors include flagellum, pilus, LPS and secreted factors, including extracellular products, type III secretion proteins, quorum-sensing molecules, and alginate.
<b>Figure 4.</b>
Figure 4.
Host responses to P. aeruginosa. Airway epithelial cells, macrophages, neutrophils, and lymphocytes release mediators that enable the host to mount a response to the invading bacteria. IL = interleukin; MIP = macrophage inflammatory protein; NADPH = nicotinamide adenine dinucleotide phosphate-reduced; RNI = reactive nitrogen intermediates; ROS = reactive oxygen species; TLR = Toll-like receptor; TNF-α = tumor necrosis factor α.
<b>Figure 5.</b>
Figure 5.
Interaction of P. aeruginosa and individual bacterial products with important receptors on airway epithelial cells.
<b>Figure 6.</b>
Figure 6.
Distribution of bacterial receptors. AsialoGM1 (red) and green fluorescent protein–labeled P. aeruginosa (green) colocalize (yellow; see arrows) at regions of cell–cell contact in polarized airway epithelial cells.
See this image and copyright information in PMC

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