8-11-14-eicosatrienoic-acid and Lung-Diseases

8-11-14-eicosatrienoic-acid has been researched along with Lung-Diseases* in 2 studies

Other Studies

2 other study(ies) available for 8-11-14-eicosatrienoic-acid and Lung-Diseases

Article	Year
Pseudomonas aeruginosa sabotages the generation of host proresolving lipid mediators. Proceedings of the National Academy of Sciences of the United States of America, 2017, 01-03, Volume: 114, Issue:1 Recurrent Pseudomonas aeruginosa infections coupled with robust, damaging neutrophilic inflammation characterize the chronic lung disease cystic fibrosis (CF). The proresolving lipid mediator, 15-epi lipoxin A Topics: 8,11,14-Eicosatrienoic Acid; Bacterial Proteins; Bronchoalveolar Lavage Fluid; Cell Line; Crystallography, X-Ray; Cystic Fibrosis; Humans; Inflammation; Lipoxins; Lung Diseases; Neutrophil Activation; Neutrophils; Pseudomonas aeruginosa; Pseudomonas Infections; Retrospective Studies; Virulence Factors	2017
Systemic disease during Streptococcus pneumoniae acute lung infection requires 12-lipoxygenase-dependent inflammation. Journal of immunology (Baltimore, Md. : 1950), 2013, Nov-15, Volume: 191, Issue:10 Acute pulmonary infection by Streptococcus pneumoniae is characterized by high bacterial numbers in the lung, a robust alveolar influx of polymorphonuclear cells (PMNs), and a risk of systemic spread of the bacterium. We investigated host mediators of S. pneumoniae-induced PMN migration and the role of inflammation in septicemia following pneumococcal lung infection. Hepoxilin A3 (HXA3) is a PMN chemoattractant and a metabolite of the 12-lipoxygenase (12-LOX) pathway. We observed that S. pneumoniae infection induced the production of 12-LOX in cultured pulmonary epithelium and in the lungs of infected mice. Inhibition of the 12-LOX pathway prevented pathogen-induced PMN transepithelial migration in vitro and dramatically reduced lung inflammation upon high-dose pulmonary challenge with S. pneumoniae in vivo, thus implicating HXA3 in pneumococcus-induced pulmonary inflammation. PMN basolateral-to-apical transmigration in vitro significantly increased apical-to-basolateral transepithelial migration of bacteria. Mice suppressed in the expression of 12-LOX exhibited little or no bacteremia and survived an otherwise lethal pulmonary challenge. Our data suggest that pneumococcal pulmonary inflammation is required for high-level bacteremia and systemic infection, partly by disrupting lung epithelium through 12-LOX-dependent HXA3 production and subsequent PMN transepithelial migration. Topics: 8,11,14-Eicosatrienoic Acid; Animals; Arachidonate 12-Lipoxygenase; Bacillus subtilis; Bacteremia; Cell Line, Tumor; Cell Movement; Chemotactic Factors; Humans; Inflammation; Lung; Lung Diseases; Mice; Mice, Inbred C57BL; Mice, Knockout; Neutrophils; Pneumococcal Infections; Streptococcus pneumoniae; Transendothelial and Transepithelial Migration	2013

Article

Year

Pseudomonas aeruginosa sabotages the generation of host proresolving lipid mediators.

Proceedings of the National Academy of Sciences of the United States of America, 2017, 01-03, Volume: 114, Issue:1

Recurrent Pseudomonas aeruginosa infections coupled with robust, damaging neutrophilic inflammation characterize the chronic lung disease cystic fibrosis (CF). The proresolving lipid mediator, 15-epi lipoxin A

Topics: 8,11,14-Eicosatrienoic Acid; Bacterial Proteins; Bronchoalveolar Lavage Fluid; Cell Line; Crystallography, X-Ray; Cystic Fibrosis; Humans; Inflammation; Lipoxins; Lung Diseases; Neutrophil Activation; Neutrophils; Pseudomonas aeruginosa; Pseudomonas Infections; Retrospective Studies; Virulence Factors

2017

Systemic disease during Streptococcus pneumoniae acute lung infection requires 12-lipoxygenase-dependent inflammation.

Journal of immunology (Baltimore, Md. : 1950), 2013, Nov-15, Volume: 191, Issue:10

Acute pulmonary infection by Streptococcus pneumoniae is characterized by high bacterial numbers in the lung, a robust alveolar influx of polymorphonuclear cells (PMNs), and a risk of systemic spread of the bacterium. We investigated host mediators of S. pneumoniae-induced PMN migration and the role of inflammation in septicemia following pneumococcal lung infection. Hepoxilin A3 (HXA3) is a PMN chemoattractant and a metabolite of the 12-lipoxygenase (12-LOX) pathway. We observed that S. pneumoniae infection induced the production of 12-LOX in cultured pulmonary epithelium and in the lungs of infected mice. Inhibition of the 12-LOX pathway prevented pathogen-induced PMN transepithelial migration in vitro and dramatically reduced lung inflammation upon high-dose pulmonary challenge with S. pneumoniae in vivo, thus implicating HXA3 in pneumococcus-induced pulmonary inflammation. PMN basolateral-to-apical transmigration in vitro significantly increased apical-to-basolateral transepithelial migration of bacteria. Mice suppressed in the expression of 12-LOX exhibited little or no bacteremia and survived an otherwise lethal pulmonary challenge. Our data suggest that pneumococcal pulmonary inflammation is required for high-level bacteremia and systemic infection, partly by disrupting lung epithelium through 12-LOX-dependent HXA3 production and subsequent PMN transepithelial migration.

Topics: 8,11,14-Eicosatrienoic Acid; Animals; Arachidonate 12-Lipoxygenase; Bacillus subtilis; Bacteremia; Cell Line, Tumor; Cell Movement; Chemotactic Factors; Humans; Inflammation; Lung; Lung Diseases; Mice; Mice, Inbred C57BL; Mice, Knockout; Neutrophils; Pneumococcal Infections; Streptococcus pneumoniae; Transendothelial and Transepithelial Migration

2013