Cytokine-induced, nitric oxide-dependent, intracellular antirickettsial activity of mouse endothelial cells.

Abstract

In a murine model of rickettsial disease in which, as in human rickettsioses, endothelial cells are the major target of infection, depletion of IFN-gamma or TNF-alpha converts a sublethal infection into a uniformly fatal disease with overwhelming rickettsial growth and decreased nitric oxide (NO) synthesis. The kinetics of NO production and rickettsial… (More)

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