The production of elevated levels of NO can have pathological consequences for the host as NO is toxic to host cells as well as microorganisms. Dis-regulated production of NO during an inflammatory response to infection or allergens may cause severe damage to host tissues. In addition, under conditions where there is an autoimmune recognition of host tissues NO may mediate the actual tissue damage observed.
The induction of toxic shock in mice after injection with LPS can be prevented by treatment with L-NMMA and, similarly, iNOS 'knockout' mice recover from LPS-induced shock while normal littermates do not, indicating that a pathogenic role can be attributed to NO production in response to bacterial products. In addition to toxic shock, the disregulated production of NO has been demonstrated to contribute to the pathology associated with neurodegenerative and inflammatory disorders.
Self-recognition and the induction of autoimmune aggression may cause the production of NO which causes damage to cells within the inflammatory focus. NO has been implicated in the tissue damage observed in several models of autoimmune disease, including autoimmune diabetes and rheumatoid arthritis. In addition, intestinal enteropathy associated with graft-versus-host disease, which involves recognition of host tissues by grafted immune cells, also depends on the induction of NO, as L-NMMA treatment in a mouse model of this disease reduces gut damage.
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