Endothelial cells and the airway

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TNFa induces hyperresponsiveness in the airway. In the lung, TNFa is performed and directly released upon stimulation from mast cells and produced by alveolar macrophages. Interestingly, TNFa inhibits surfactant protein C gene transcription, which may be a critical factor in a number of infections and diseases with production of high levels of TNFa. In asthma, TNFa is upregulated and can be detected in the sputum of patients with acute attacks. Influenza A viral pneumonia is mediated by TNFa, and anti-

TNFa treatment of mice prolongs survival without reducing the virus titer.

TNFa induces cell-cell dissociation of endothelial cells and reduces intracellular cAMP and glutathione levels, resulting in increased permeability of the endothelial cell barrier. TNFct also alters the responsiveness of airway smooth muscle cells.

See also: Acquired immune deficiency syndrome (AIDS); Apoptosis; Autoimmune diseases; Autoimmunity; Bacteria, immunity to; Cytokine assays; Cytokine genes, regulation of; Cytokine receptors, soluble; Cytokine receptors; Cytotoxicity, mechanisms of; Endotoxin (lipopolysaccharide (LPS)); Fas (CD95) and fas iigand; Graft rejection; Immunopathol-ogy; insulin-dependent diabetes mellitus, animal models; Insulin-dependent diabetes mellitus, human; Macrophage activation; Malaria; Mixed lymphocyte reaction (MLR); Rheumatoid arthritis, animal models; Rheumatoid arthritis, human; Schistosomiasis; Septic shock; Superantigens; Transplantation; Lym-photoxin; TNF receptors; Tumors, immune response to.

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