Vouldoukis I, Drapier J C, Nüssler A K, Tselentis Y, Da Silva O A, Gentilini M, Mossalayi D M, Monjour L, Dugas B
Laboratoire de Parasitologie Experimentale, Faculté de Médecine Pitié Salpétrière, Paris, France.
Antimicrob Agents Chemother. 1996 Jan;40(1):253-6. doi: 10.1128/AAC.40.1.253.
Following successful chemotherapy in canine visceral leishmaniasis, monocyte-derived macrophages can induce antileishmanial activity via a gamma interferon-dependent mechanism in the presence of autologous lymphocytes. The killing of leishmania correlated with the induction of the NO synthase pathway, because it correlated with the generation of nitrogen derivative production and was abrogated in the presence of NG-monomethyl-L-arginine, a competitive inhibitor of the NO synthase pathway. The level of L-citrulline in serum, which was produced after activation of the NO synthase pathway, was markedly enhanced in dogs receiving successful chemotherapy. Taken together, these data indicate that following successful chemotherapy of visceral leishmaniasis, leishmania parasites are killed by macrophages activated by gamma interferon-producing lymphocytes via an NO-dependent mechanism.
在犬内脏利什曼病化疗成功后，单核细胞衍生的巨噬细胞在自体淋巴细胞存在的情况下，可通过γ干扰素依赖性机制诱导抗利什曼原虫活性。利什曼原虫的杀伤与一氧化氮合酶途径的诱导相关，因为它与氮衍生物的产生相关，并且在一氧化氮合酶途径的竞争性抑制剂NG-单甲基-L-精氨酸存在时被消除。在接受成功化疗的犬中，一氧化氮合酶途径激活后产生的血清L-瓜氨酸水平显著升高。综上所述，这些数据表明，在内脏利什曼病化疗成功后，利什曼原虫被产生γ干扰素的淋巴细胞激活的巨噬细胞通过一氧化氮依赖性机制杀死。
