PPARα downregulates airway inflammation induced by lipopolysaccharide in the mouse

@article{DelayreOrthez2005PPARDA,
  title={PPAR$\alpha$ downregulates airway inflammation induced by lipopolysaccharide in the mouse},
  author={C. Delayre-Orthez and J. Becker and I. Guénon and V. Lagente and J. Auwerx and N. Frossard and F. Pons},
  journal={Respiratory Research},
  year={2005},
  volume={6},
  pages={91 - 91}
}
BackgroundInflammation is a hallmark of acute lung injury and chronic airway diseases. In chronic airway diseases, it is associated with profound tissue remodeling. Peroxisome proliferator-activated receptor-α (PPARα) is a ligand-activated transcription factor, that belongs to the nuclear receptor family. Agonists for PPARα have been recently shown to reduce lipopolysaccharide (LPS)- and cytokine-induced secretion of matrix metalloproteinase-9 (MMP-9) in human monocytes and rat mesangial cells… Expand
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  • Medicine
  • iScience
  • 2021
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References

SHOWING 1-10 OF 51 REFERENCES
PPAR‐γ agonists as therapy for diseases involving airway neutrophilia
TLDR
If a peroxisome proliferator-activated receptor agonist has the same effect in man, and neutrophils are important in the progression of respiratory diseases, such as chronic obstructive pulmonary disease, then this class of compounds could be a potential therapy. Expand
PPAR-gamma agonists as therapy for diseases involving airway neutrophilia.
TLDR
If a peroxisome proliferator-activated receptor agonist has the same effect in man, and neutrophils are important in the progression of respiratory diseases, such as chronic obstructive pulmonary disease, then this class of compounds could be a potential therapy. Expand
Peroxisome Proliferator–activated Receptors α and γ Down-regulate Allergic Inflammation and Eosinophil Activation
TLDR
PPARs, PPAR-α and -γ are expressed in eosinophils and their activation inhibits in vitro chemotaxis and antibody-dependent cellular cytotoxicity, and might be of therapeutic interest for the regulation of allergic or inflammatory reactions by targeting both regulatory and effector cells involved in the immune response. Expand
Role for macrophage inflammatory protein-2 in lipopolysaccharide-induced lung injury in rats.
TLDR
Data indicate that MIP-2 plays a significant role in LPS-induced inflammatory response in rat lungs and is required for the full recruitment of neutrophils. Expand
Regulation of macrophage chemokine expression by lipopolysaccharide in vitro and in vivo.
TLDR
Findings indicate that selective regulation of chemokine expression in vivo may result from differential response of macrophages to pro- and antiinflammatory stimuli and to cell type-specific patterns of stimulus sensitivity, and suggest that individual chemokines are differentially regulated in response to LPS. Expand
Role of the type 1 TNF receptor in lung inflammation after inhalation of endotoxin or Pseudomonas aeruginosa.
TLDR
TNFR1 facilitates neutrophil recruitment after inhalation of lipopolysaccharide, in part by augmenting chemokine induction, and attenuates lung inflammation in response to live bacteria but does not contribute to increased lung permeability and is not required for the elimination of P. aeruginosa. Expand
Peroxisome Proliferator-activated Receptor α Negatively Regulates the Vascular Inflammatory Gene Response by Negative Cross-talk with Transcription Factors NF-κB and AP-1*
TLDR
Fibrates inhibit the vascular inflammatory response via PPARα by interfering with the NF-κB and AP-1 transactivation capacity involving direct protein-protein interaction with p65 and c-Jun. Expand
Activation of Proliferator-activated Receptors α and γ Induces Apoptosis of Human Monocyte-derived Macrophages*
TLDR
It is shown that the PPARα and PPARγ forms are expressed in differentiated human monocyte-derived macrophages, which participate in inflammation control and atherosclerotic plaque formation and demonstrate a novel function of PPAR in human macrophage with likely consequences in inflammation and Atherosclerosis. Expand
Regulation of monocyte chemoattractant protein-1 gene expression and secretion in rat pulmonary alveolar macrophages by lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-1 beta.
TLDR
The results suggest that resident PAMs, through elaboration of MCP-1, may play a pivotal role in regulating recruitment and activation of monocytes in the lung during acute inflammatory lung injury. Expand
Activation of PPARα or γ Reduces Secretion of Matrix Metalloproteinase 9 but Not Interleukin 8 from Human Monocytic THP-1 Cells
TLDR
It is shown that PPARα (fenofibrate) or PPARγ (rosiglitazone) agonists failed to modulate LPS-induced secretion of IL-8 in THP-1 cells, suggesting that PPar may regulate only a subset of the proinflammatory genes controlled by AP-1, STAT, and NF-κB. Expand
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