Trichostatin A, a histone deacetylase inhibitor, down-regulates interleukin-12 transcription in SV-40-transformed lung epithelial cells

Interleukin-8 Expression Is Regulated by Histone Deacetylases through the Nuclear Factor-κB Pathway in Breast Cancer

“…However, it is worth mentioning that, in most instances, HDAC inhibitors were acting mainly in cooperation with other inducers of IL-8 gene expression. This is the case for the synergy between HDAC inhibitors and IL-1␤ (Ito et al, 2001;Wen and Wu, 2001;Böcker et al, 2003) or TNF-␣ (Ashburner et al, 2001;Iwata et al, 2002;Adam et al, 2003). On the other hand, in some cell types, IL-8 expression is even down-regulated by HDAC inhibitors (Hoshimoto et al, 2002;Iwata et al, 2002).…”

Endoplasmic Reticulum Stress Induced by Surfactant Protein C BRICHOS Mutants Promotes Proinflammatory Signaling by Epithelial Cells

“…These effects include histone deactylase inhibition (HDACi) (41)(42)(43) and enhanced MAPK (JNK) signaling (44). The treatment of cells with other inducers of HDACi in vitro (such as trichostatin A) was shown to modulate IL-8 production in both an NFkB-dependent and AP-1-dependent fashion, but this effect is highly cell-specific (33,45). In addition, Roque and colleagues observed that 4-PBA enhances the production of IL-8 in lung epithelial cells expressing DF508-CFTR (44).…”

Proinflammatory Effect of Sodium 4-Phenylbutyrate in ΔF508-Cystic Fibrosis Transmembrane Conductance Regulator Lung Epithelial Cells: Involvement of Extracellular Signal-Regulated Protein Kinase 1/2 and c-Jun-NH2-Terminal Kinase Signaling

“…The question of whether HDACi stimulates or inhibits inflammatory gene expression is still under debate, because studies have shown that many genes are suppressed or induced according to the cell types and stimuli (Adcock, 2007;Ito et al, 2007). Thus, trichostatin A enhanced lipopolysaccharide-stimulated IL-8, but it repressed IL-12 expression in the normal BEAS-2B bronchial cell line (Iwata et al, 2002). A recent study showed that IB3-1 cells that were treated with 5 mM 4-PBA for 24 h down-regulated transcript levels of cyclooxygenase-2 and IL-6 but not IL-8 (Vij et al, 2008).…”