Pseudomonas Invasion of Type I Pneumocytes Is Dependent on the Expression and Phosphorylation of Caveolin-2*

@article{Zaas2005PseudomonasIO,
  title={Pseudomonas Invasion of Type I Pneumocytes Is Dependent on the Expression and Phosphorylation of Caveolin-2*},
  author={David W. Zaas and Mathew J Duncan and Guojie Li and Jo Rae Wright and Soman N. Abraham},
  journal={Journal of Biological Chemistry},
  year={2005},
  volume={280},
  pages={4864 - 4872}
}
Pseudomonas aeruginosa is a major cause of pneumonia in patients with cystic fibrosis and other immuncompromising conditions. Here we showed that P. aeruginosa invades type I pneumocytes via a lipid raft-mediated mechanism. P. aeruginosa invasion of rat primary type I-like pneumocytes as well as a murine lung epithelial cell line 12 (MLE-12) is inhibited by drugs that remove membrane cholesterol and disrupt lipid rafts. Confocal microscopy demonstrated co-localization of intracellular P… Expand
Counteracting Signaling Activities in Lipid Rafts Associated with the Invasion of Lung Epithelial Cells by Pseudomonas aeruginosa*
TLDR
Pseudomonas aeruginosa has the capacity to invade lung epithelial cells by co-opting the intrinsic endocytic properties of lipid rafts, which are rich in cholesterol, sphingolipids, and proteins, such as caveolin-1 and -2, and there also exists in these cells an intrinsic Csk-dependent cellular defense mechanism aimed at impairing this activity. Expand
Caveolin-1 Modifies the Immunity to Pseudomonas aeruginosa
TLDR
P. aeruginosa colonized cav1 KO mice much better compared with the wild-type controls in a model of chronic infection, indicting an important contribution of Cav-1 to innate host immunity to P. aerUGinosa infection. Expand
The Role of Lipid Raft Aggregation in the Infection of Type II Pneumocytes by Mycobacterium tuberculosis
TLDR
Evidence is provided for significant mycobacterial-induced changes in the plasma membrane of alveolar epithelial cells and that Mtb strains vary in their ability to facilitate aggregation and utilization of LR. Expand
Elevated Inflammatory Response in Caveolin-1-deficient Mice with Pseudomonas aeruginosa Infection Is Mediated by STAT3 Protein and Nuclear Factor κB (NF-κB)*
TLDR
It is indicated that Cav-1 is critical for inflammatory responses regulating the STAT3/NF-κB pathway and thereby impacting P. aeruginosa infection. Expand
Cystic fibrosis transmembrane conductance regulator and caveolin-1 regulate epithelial cell internalization of Pseudomonas aeruginosa.
TLDR
Efficient initiation of innate immunity to P. aeruginosa requires formation of an epithelial "internalization platform" involving both caveolin-1 and functional, laterally mobile CFTR. Expand
Role of Caveolin Proteins in Sepsis.
  • G. Sowa
  • Biology, Medicine
  • Pediatrics & therapeutics : current research
  • 2012
TLDR
New exciting discoveries related to the specific role of caveolin-1 and the less studied Caveolin-2 in regulating signaling and outcome associated with sepsis induced by LPS and pathogenic bacteria at molecular, cellular and systemic levels are discussed. Expand
Glycolipid-Dependent, Protease Sensitive Internalization of Pseudomonas aeruginosa Into Cultured Human Respiratory Epithelial Cells
TLDR
Internalization of PAK strain Pseudomonas aeruginosa into human respiratory epithelial cell lines and HeLa cervical cancer cells in vitro was readily demonstrable via a gentamycin protection assay and was markedly enhanced by target cell pretreatment with the exogenous GSL, deacetyl gangliotetraosyl ceramide (Gg4). Expand
Trafficking of Mycobacterium tuberculosis bacilli in type II pneumocytes
TLDR
Data suggest that Mtb has the ability to alter the epithelial cell autophagy pathway to support infection by the bacterium, and strongly suggest that M. tuberculosis employs numerous strategies for survival and replication which are unique to the particular host cell infected. Expand
Cellular responses of A549 alveolar epithelial cells to serially collected Pseudomonas aeruginosa from cystic fibrosis patients at different stages of pulmonary infection.
TLDR
These findings suggest that despite the loss of virulence factors during the adaptation process in the CF lung by late P. aeruginosa strains, they retain high proinflammatory abilities that likely contribute to the disease pathogenesis. Expand
Src kinase Lyn is crucial for Pseudomonas aeruginosa internalization into lung cells
TLDR
It is demonstrated that Lyn activation by phosphorylation significantly impacted invasion of an alveolar epithelial cell line, primary lung cells, and rat lungs by Pseudomonas aeruginosa, a common opportunistic lung pathogen affecting individuals with deficient lung immunity. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 45 REFERENCES
Bacterial Penetration of Bladder Epithelium through Lipid Rafts*
TLDR
Type 1 fimbriated Escherichia coli represents the most common human uropathogen, owing much of its virulence to invasion of the uroepithelium, which, paradoxically, contribute to bladder impermeability. Expand
Host defense against Pseudomonas aeruginosa requires ceramide-rich membrane rafts
TLDR
This work shows that ceramide-enriched membrane platforms are central to the host defense against this potentially lethal pathogen P. aeruginosa. Expand
Infectivity of Legionella pneumophila mip mutant for alveolar epithelial cells
TLDR
Data indicate that Mip enhances infection of pneumocytes and that L. pneumophila employs some of the same genes (mechanisms) to infect epithelial cells and marcophages. Expand
Localization of Cystic Fibrosis Transmembrane Conductance Regulator to Lipid Rafts of Epithelial Cells Is Required for Pseudomonas aeruginosa-Induced Cellular Activation 1
TLDR
Results indicate that lipid raft localization of CFTR is required for signaling in response to P. aeruginosa lung infection, a process that is defective in CF. Expand
Type 1 pilus‐mediated bacterial invasion of bladder epithelial cells
TLDR
The results demonstrate that UPEC strains are not strictly extracellular pathogens and that the type 1 pilus adhesin FimH can directly trigger host cell signaling cascades that lead to bacterial internalization. Expand
Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities.
TLDR
The results indicate that eNOS activity is up-regulated in Cav-1 null animals, and this activity can be blunted by using a specific NOS inhibitor, nitro-l-arginine methyl ester. Expand
Caveolin-1 expression and caveolae biogenesis during cell transdifferentiation in lung alveolar epithelial primary cultures.
TLDR
It is demonstrated that freshly isolated rat ATII cells lack Caveolae and expression of caveolin-1 (a critical caveolae structural protein) as a function of in vitro transformation from the ATII to the ATI-like phenotype. Expand
Induction and evasion of host defenses by type 1-piliated uropathogenic Escherichia coli.
TLDR
Bacterial attachment resulted in exfoliation of host bladder epithelial cells as part of an innate host defense system through a rapid apoptosis-like mechanism involving caspase activation and host DNA fragmentation. Expand
Pathogenesis of septic shock in Pseudomonas aeruginosa pneumonia.
TLDR
The results demonstrate the importance of compartmentalization of inflammatory mediators in the lung, and the crucial role of bacterial cytotoxins in causing alveolar epithelial damage in the pathogenesis of acute septic shock in P. aeruginosa pneumonia. Expand
Microbial entry through caveolae: variations on a theme
TLDR
It seems that, though a wide variety of microorganisms are capable of utilizing caveolae/lipid rafts in various stages of their intracellular lifestyle, there can be distinct differences in how each microbe interacts with these structures. Expand
...
1
2
3
4
5
...