c-Jun N-terminal kinase negatively regulates dsRNA and RSV induction of tumor necrosis factor- alpha transcription in human epithelial cells.

Secretion of inflammatory cytokines is the initial step of the immune response to viral infections. This innate immune response is mediated by the expression of a variety of cytokines, exemplified by tumor necrosis factor- alpha (TNF-alpha). The presence of dsRNA during viral infections is a key step in activation of several signaling pathways, including protein kinase R (PKR), toll-like receptor 3 (TLR3), mitogen-activated protein kinase (MAPK), activator protein-1 (AP-1), interferon regulatory factors (IRFs), and NF-kappaB pathways, which are all relevant in the expression of inflammatory cytokines.

Viral induction of inflammatory cytokines in human epithelial cells follows a p38 mitogen-activated protein kinase-dependent but NF-kappa B-independent pathway.

The initial step in an immune response toward a viral infection is the induction of inflammatory cytokines. This innate immune response is mediated by expression of a variety of cytokines exemplified by TNF-alpha and IL-1beta. A key signal for the recognition of intracellular viral infections is the presence of dsRNA.

Protein kinase R regulates double-stranded RNA induction of TNF-alpha but not IL-1 beta mRNA in human epithelial cells.

Epithelial cells represent the initial site of respiratory viral entry and the first line of defense against such infections. This early antiviral response is characterized by an increase in the production of proinflammatory cytokines such as TNF-alpha and IL-1 beta. dsRNA, which is a common factor present during the life cycle of both DNA and RNA viruses, is known to induce TNF-alpha and IL-1 beta in a variety of cells.