PMID: 16521860Mar 9, 2006Paper

Role of reactive nitrogen species in development of hepatic injury in a C57bl/6 mouse model of human granulocytic anaplasmosis

Comparative Medicine
Michelle D BrowningDiana G Scorpio

Abstract

Human granulocytic anaplasmosis (HGA), caused by the granulocytic rickettsia-like organism Anaplasma phagocytophilum, is the 3rd most frequent vector-borne infection in North America. To understand the disease mechanisms of HGA, we developed a murine model that lacks clinical disease yet exhibits characteristic histopathologic and immunologic changes. Because the degree of hepatic histopathology is unrelated to high bacterial numbers, tissue injury in HGA is thought to occur due to products of innate immunity, such as nitric oxide (NO) and reactive nitrogen species (RNS) from cytokine-activated macrophages. To test the hypothesis that RNS cause hepatic tissue damage, mice received either water treated with a nonspecific inhibitor of inducible nitric oxide synthase, L-NAME, or untreated water for 7 to 10 d before infection and continuing thereafter. Mice were euthanized for tissue harvest at 0, 7, 14, or 21 d after infection to assess differences in histopathology, hepatic bacterial load, RNS quantity in urine and liver, and serum chemistry values. Overall, L-NAME treatment had a beneficial effect, resulting in lower histopathology scores and RNS levels compared with those of untreated mice. There were no significant differences...Continue Reading

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