Infection and Activation of Airway Epithelial Cells by<i>Chlamydia pneumoniae</i>

Jahn, H; Krüll, Matthias; Wuppermann, Frederik N.; Klucken, Andrea C.; Rosseau, Simone; Seybold, Joachim; Hegemann, Johannes H.; Jantos, Christian A.; Suttorp, Norbert

doi:10.1086/317608

Cited by 62 publications

(59 citation statements)

References 58 publications

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“…One aspect of the inflammatory process involves the infiltration of lung tissue by neutrophils (2,5,6,8,33). Neutrophils are capable of crossing both the endothelial and epithelial barriers in response to an infection in the airspace (8).…”

Section: Discussionmentioning

confidence: 99%

“…Several bacterial species have been implicated as causes of pneumonia, including Streptococcus pneumoniae, Chlamydia pneumoniae, Haemphilus influenzae, Klebsiella pneumoniae, Legionella pneumophila, Escherichia coli, and Pseudomonas aeruginosa (1,(3)(4)(5). Pseudomonas aeruginosa (PA) 3 is the bacterial pathogen most associated with lung damage due to inflammation in individuals with cystic fibrosis (2).…”

Section: Iseases Involving Bacterial-induced Lung Inflammationmentioning

confidence: 99%

“…Although there are numerous reports of various bacterial products capable of inducing IL-8 secretion in several different primary and transformed airway epithelial cell lines (5,6,11,12), it is unclear at present whether epithelial IL-8 production by lung epithelial cells is sufficient for mediating transepithelial PMN migration. Thus, the objective of this study was to specifically investigate the molecular mechanisms that are responsible for the final step of PMN recruitment during bacterial infection, namely, PMN transepithelial transmigration using a reductionistic in vitro model.…”

Section: Iseases Involving Bacterial-induced Lung Inflammationmentioning

confidence: 99%

“…IL-8 is a well-known PMN chemoattractant that is secreted by the epithelial cells of several mucosal surfaces upon interaction with bacteria (5,11,20,21). The signaling cascade leading to IL-8 secretion has been well studied and thought to represent an innate response by mucosal surfaces upon the sensing of infection (2,26,27).…”

Section: Pathogenic Bacteria Induce Il-8 Secretionmentioning

confidence: 99%

“…Taking together all of the above data, we hypothesize that although IL-8 is produced in response to bacterial infection, IL-8 is not responsible for the specific step of transepithelial migration of PMNs to the airway lumen. Rather IL-8 is more likely required for the recruitment of PMNs from the blood stream through the interstitial space (5,8,20,22). Hence, PMN transepithelial migration must involve a distinct PMN chemoattractant.…”

Section: Map/erk Inhibitors Do Not Block Bacterial-induced Pmn Transmmentioning

confidence: 99%

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Polymorphonuclear Cell Transmigration Induced by Pseudomonas aeruginosa Requires the Eicosanoid Hepoxilin A3

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The Journal of Immunology

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Lung inflammation resulting from bacterial infection of the respiratory mucosal surface in diseases such as cystic fibrosis and pneumonia contributes significantly to the pathology. A major consequence of the inflammatory response is the recruitment and accumulation of polymorphonuclear cells (PMNs) at the infection site. It is currently unclear what bacterial factors trigger this response and exactly how PMNs are directed across the epithelial barrier to the airway lumen. An in vitro model consisting of human PMNs and alveolar epithelial cells (A549) grown on inverted Transwell filters was used to determine whether bacteria are capable of inducing PMN migration across these epithelial barriers. A variety of lung pathogenic bacteria, including Klebsiella pneumoniae, Escherichia coli, and Pseudomonas aeruginosa are indeed capable of inducing PMN migration across A549 monolayers. This phenomenon is not mediated by LPS, but requires live bacteria infecting the apical surface. Bacterial interaction with the apical surface of A549 monolayers results in activation of epithelial responses, including the phosphorylation of ERK1/2 and secretion of the PMN chemokine IL-8. However, secretion of IL-8 in response to bacterial infection is neither necessary nor sufficient to mediate PMN transepithelial migration. Instead, PMN transepithelial migration is mediated by the eicosanoid hepoxilin A3, which is a PMN chemoattractant secreted by A549 cells in response to bacterial infection in a protein kinase C-dependent manner. These data suggest that bacterial-induced hepoxilin A3 secretion may represent a previously unrecognized inflammatory mechanism occurring within the lung epithelium during bacterial infections.

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