GEO DataSets

(Submitter supplied) Background: Ozone (O3) is the predominant oxidant air pollutant associated with respiratory inflammation, lung dysfunction, and worsening preexisting airway diseases. We determined that TNFR signlaing pathway plays a key role in lung injury and inflammation caused by O3 in mice. However, downstream molecular mechanisms underlying TNFR pathway have not been investigated. Methods: To investigate the role of TNFR pathway in gene expression changes, Tnfr1/2-deficient (Tnfr-/-) and wild-type (Tnfr+/+, C57BL/6J) mice were exposed to air or 0.3-ppm O3. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL339

24 Samples

Download data: CEL, CHP

(Submitter supplied) Background: Ozone (O3) is the predominant oxidant air pollutant associated with respiratory inflammation, lung dysfunction, and worsening preexisting airway diseases. We previously determined that lack of NF-kB signlaing pathway suppressed lung injury and inflammation caused by O3 in mice. The current study was to determine transcriptome mechanisms orchestrated by NF-kB during the development of pulmonary O3 injury. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

12 Samples

Download data: CEL, CHP

(Submitter supplied) We previously identified toll-like receptor 4 (Tlr4) as a candidate gene responsible for ozone (O3)-induced pulmonary hyperpermeability and inflammation. The objective of this study was to determine the mechanism through which TLR4 modulates O3-induced pulmonary responses and to utilize transcriptomics to determine TLR4 effector molecules. C3H/HeJ (HeJ; Tlr4 mutant) and C3H/HeOuJ (OuJ; Tlr4 normal), mice were exposed continuously to 0.3 ppm O3 or filtered air for 6, 24, 48 or 72 hr. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS4585

Platform:

GPL339

24 Samples

Download data: CEL

Analysis of lung from Toll-like receptor 4 (Tlr4)-deficient, C3H/HeJ males exposed to 0.3 ppm ozone (O3) for up to 48hr. Tlr4 is involved in O3-induced pulmonary hyperpermeability and inflammation. Results provide insight into the molecular basis of Tlr4 modulation of O3-induced pulmonary responses.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent, 2 genotype/variation, 2 strain, 4 time sets

Platform:

GPL339

Series:

GSE20715

24 Samples

Download data: CEL

(Submitter supplied) Ozone is a common pollutant and a potent oxidant in industrialized nations. The mechanisms of ozone-induced lung injury and differential susceptibility are not fully understood. Ozone-induced lung inflammation is mediated, in part, by the innate immune system. We hypothesized that mannose binding lectin (MBL), which has a central role in the activation of the complement pathway of innate immunity, is a necessary component of the pro-inflammatory events caused by ozone-mediated activation of the innate immune system. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL4134

39 Samples

Download data: TXT