Histamine H1-receptor antagonists inhibit nuclear factor-kappaB and activator protein-1 activities via H1-receptor-dependent and -independent mechanisms.

Background: Histamine H1-receptor antagonists are used to relieve the symptoms of an immediate allergic reaction. They have additional anti-inflammatory effects that could result from an inhibition of the transcription factors activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB). The implication of the H1-receptor in these effects is controversial.

Differential regulation of RANTES and IL-8 expression in lung adenocarcinoma cells.

In lung adenocarcinoma, expression of Regulated upon Activation, Normal T cell Expressed and presumably Secreted (RANTES) is a predictor of survival while that of interleukin (IL)-8 is associated with a poor prognosis. In several models, tumorigenesis is abolished by RANTES, while it is facilitated by IL-8. We studied the regulation of RANTES and IL-8 expression in A549 lung adenocarcinoma cells.

IL-10 promoter and IL4-Ralpha gene SNPs are associated with immediate beta-lactam allergy in atopic women.

Background: Allergic reactions to beta-lactam antibiotics represent the most frequent cause of immunological drug reactions.

Objective: This study evaluates the involvement of genetic susceptibility factors in patients with immediate allergic reactions to beta-lactams. We examined 15 single nucleotide polymorphisms (SNP) of genes coding proteins implicated in immunoglobulin (Ig)E synthesis regulation.

[Glucocorticoids and their receptor: mechanisms of action and clinical implications].

Background: Glucocorticoids are used as anti-inflammatory, immuno-modulatory, anti-proliferative and cytotoxic drugs, but they also trigger important side-effects. These hormones bind to glucocorticoid receptor alpha (GRalpha), an intracellular protein, which acts essentially in the nucleus.

Main Points: GRalpha is a ligand-activated transcription factor that positively or negatively regulates gene expression by distinct mechanisms.

Persistent activation of nuclear factor-kappaB signaling pathway in severe uncontrolled asthma.

The transcription factor nuclear factor-kappaB (NF-kappaB) is inactive when bound to its inhibitory protein IkappaBalpha. On cell stimulation with inflammatory signals, IkappaBalpha is phosphorylated by IkappaB kinases and subsequently degraded. Freed NF-kappaB then induces expression of cytokines such as granulocyte-macrophage colony-stimulating factor, interleukin-8, and regulated upon activation, normal T cell expressed and secreted.