GEO DataSets

Analysis of laser-microdissected airway epithelial cells from snap-frozen lung 0 and 2 days after lipopolysaccharide (LPS) exposure. Inhalation of LPS can lead to chronic lung diseases like cystic fibrosis and asthma. Results provide insight into inflammatory mediators modulated by LPS exposure.

Organism:

Rattus norvegicus

Type:

Expression profiling by array, count, 2 time sets

Platform:

GPL85

Series:

GSE36174

6 Samples

Download data: CEL, CHP, TXT

(Submitter supplied) Acute lung inflammation can alter the pulmonary function of susceptible individuals and exacerbate the pathogenesis of chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD), cystic fibrosis and asthma. Exposure to lipopolysaccharide (LPS) or endotoxin, a constituent of outer cell membrane of gram negative bacteria, induces airway inflammation that is primarily characterized by increased polymorphonuclear neutrophils (PMNs) at early time points. more...

Organism:

Rattus norvegicus

Type:

Expression profiling by array

Dataset:

GDS4253

Platform:

GPL85

6 Samples

Download data: CEL, CHP, TXT

(Submitter supplied) Despite the appreciated in vivo role of the redox-active Pseudomonas virulence factor pyocyanin in Pseudomonas airway infections and the recognized importance of airway epithelial cells in combating bacterial pathogens, little is known about pyocyanin’s effect on airway epithelial cells. We find that exposure of bronchiolar epithelial cells to pyocyanin results in MUC2/MUC5AC induction and mucin secretion mediated by reactive oxygen species production, activation of the epidermal growth factor receptor pathway and release of inflammatory cytokines (IL-1b, IL-6, TGFa, TNFa). more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

4 Samples

Download data: TXT