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KMID : 0351219930250020091
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Korean Journal of Infectious Diseases
1993 Volume.25 No. 2 p.91 ~ p.101
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Effects of BCG Infection on the Multiplication of R. tsutsugamushi in the Mouse
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이복수
홍영권/전창덕/김인재/정헌택/박석돈/김익상/장우현
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Abstract
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It has recently been reported that gamma-interferon (INF-γ) and tumor necrosis factor (TNF) or lipopplysaccharide (LPS) activate macrophages to kill intracellular parasites by means of nitrc oxide (NO). It is now generally accepted that NO is
the
endothelium-derived relaxing factor, and that it also participates in the regulation of the nervous and immune systems. Activated macrophages form NO-2 and NO-3 from the terminal guanidino nirtogen atoms of L-arginine by a process now known to
proceed
via the formation of NO. This pathway is inhibited by the L-arginine analog (NG-monomethyl-L-arginine; NGMMA), forms L-citruliine as a co-product and is responsible for the cytotoxic action of macrophages. In this study, the authors found that
INF-γ
and/or LPS induced murine macrophages to kill Rickettsiae tsutsugamushi in vitro and macrophages from BCG-infected mice got the host resistance against R. tsutsugamushi in vitro as well as in vivo. The rickettsicidal effect induced by the
combination of
INF-γ and/or LPS can also be completely inhibited by NGMMA, leading to a dose-dependent inhibition of NO production. These data demonstrate that INF- and/or LPS as well as BCG-activated macrophages mediate host resistance against R.
tsutsugamushi
infection through NO, which is necessary for the killing of the intracellular parasite.
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KEYWORD
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