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Influenza A Virus Inhibits Type I IFN Signaling via NF-κB-Dependent Induction of SOCS-3 Expression
Data is presented indicating that influenza A viruses not only suppress IFNβ gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the suppressor of cytokine signaling-3 (SOCS-3) protein.
Neutrophil-derived S100A12 in acute lung injury and respiratory distress syndrome
S100A12 expression may reflect neutrophil activation during lung inflammation and contribute to pulmonary inflammation and endothelial activation via binding to RAGE, and are found at high concentrations in pulmonary tissue and bronchoalveolar lavage fluid in acute lung injury.
Mutations in STAT3 and diagnostic guidelines for hyper-IgE syndrome.
Staphylococcus aureus small-colony variants are adapted phenotypes for intracellular persistence.
Intracellular persistence via the development of an adapted subpopulation of SCVs most likely represents an important strategy of S. aureus to hide within the host cells, which could be a reservoir for chronic infections.
Transcriptional profiling of IKK2/NF-kappa B- and p38 MAP kinase-dependent gene expression in TNF-alpha-stimulated primary human endothelial cells.
The results define a list of primary candidates for targeted modulation of endothelial functions during inflammation and identify genes suppressed by IKK2/NF-kappa B and novel TNF-alpha-induced genes.
Keratinocytes Determine Th1 Immunity during Early Experimental Leishmaniasis
The data indicate for the first time that epidermal cytokine expression is a decisive factor in the generation of protective Th1 immunity and contributes to the outcome of infection with this important human pathogen.
Erk5 Activation Elicits a Vasoprotective Endothelial Phenotype via Induction of Krüppel-like Factor 4 (KLF4)*
Evidence is provided that constitutive Erk5 activation elicits an overall protective phenotype characterized by increased apoptosis resistance and a decreased angiogenic, migratory, and inflammatory potential, which underscore a major protective function of the MEK5/Erk5/KLF4 module in ECs and implicate agonistic ErK5 activation as potential strategy for treatment of vascular diseases.
TNF induces distinct gene expression programs in microvascular and macrovascular human endothelial cells
The establishment of EC type‐specific expression patterns may provide the basis for a selective manipulation of specific endothelial subtypes in different inflammatory diseases.
Myeloid-related proteins 8 and 14 induce a specific inflammatory response in human microvascular endothelial cells.
It is shown for the first time that MRP8/MRP14 induce a thrombogenic, inflammatory response in human microvascular endothelial cells by increasing the transcription of proinflammatory chemokines and adhesion molecules and by decreasing the expression of cell junction proteins and molecules involved in monolayer integrity.
Proinflammatory S100A12 can activate human monocytes via Toll-like receptor 4.
Human S100A12 is an endogenous TLR4 ligand that induces monocyte activation, thereby acting as an amplifier of innate immunity during early inflammation and the development of sepsis.