Acrolein Inhalation Suppresses Lipopolysaccharide-Induced Inflammatory Cytokine Production but Does Not Affect Acute Airways Neutrophilia
| Autor: | David I. Kasahara, Matthew E. Poynter, Albert van der Vliet, David R. Hemenway, Ziryan Othman |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Lipopolysaccharides
Lung Diseases Male Lipopolysaccharide Neutrophils medicine.medical_treatment Immunology Apoptosis Inflammation Article Proinflammatory cytokine Mice chemistry.chemical_compound Th2 Cells In vivo Administration Inhalation Animals Immunology and Allergy Medicine Acrolein Inhalation business.industry JNK Mitogen-Activated Protein Kinases NF-kappa B Th1 Cells Neutrophilia Mice Inbred C57BL Cytokine chemistry Acute Disease Cytokines medicine.symptom business |
| Zdroj: | The Journal of Immunology. 181:736-745 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.181.1.736 |
| Popis: | Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 μg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either before or after LPS challenge. Exposure to acrolein either before or after LPS challenge did not significantly affect the overall extent of LPS-induced lung inflammation, or the duration of the inflammatory response, as observed from recovered lung lavage leukocytes and histology. However, exposure to acrolein after LPS instillation markedly diminished the LPS-induced production of several inflammatory cytokines, specifically TNF-α, IL-12, and the Th1 cytokine IFN-γ, which was associated with reduction in NF-κB activation. Our data demonstrate that acrolein exposure suppresses LPS-induced Th1 cytokine responses without affecting acute neutrophilia. Disruption of cytokine signaling by acrolein may represent a mechanism by which smoking contributes to chronic disease in chronic obstructive pulmonary disease and asthma. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|