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首页> 外文OA文献 >Cyclophosphamide Decreases Nitrotyrosine Formation and Inhibits Nitric Oxide Production by Alveolar Macrophages in Mycoplasmosis
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Cyclophosphamide Decreases Nitrotyrosine Formation and Inhibits Nitric Oxide Production by Alveolar Macrophages in Mycoplasmosis

机译：环磷酰胺可减少硝基酪氨酸的形成并抑制肺炎性支原体肺泡巨噬细胞产生一氧化氮

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We previously reported that congenic C57BL/6 inducible nitric oxide synthase−/− (iNOS−/−) mice infected with Mycoplasma pulmonis developed higher bacterial numbers and lung lesion scores than C57BL/6 iNOS+/+ controls but had similar lung nitrotyrosine levels. The present studies investigated the role of inflammatory cells in nitrotyrosine formation during mycoplasmal infection. iNOS+/+ and iNOS−/− mice were injected with cyclophosphamide (CYP) and inoculated with 107 CFU of M. pulmonis. CYP pretreatment of M. pulmonis-infected iNOS+/+ and iNOS−/− mice reduced polymorphonuclear cells (PMNs) within bronchoalveolar lavages (BALs) by 88 and 72%, respectively, and whole-lung myeloperoxidase levels by 80 and 78%, respectively, at 72 h postinfection but did not alter the number of alveolar macrophages (AMs) in BALs. CYP treatment also significantly decreased nitrate and nitrite (NOx) levels in BALs and plasma of infected iNOS+/+ mice, whereas neither CYP nor mycoplasmal infection altered NOx in iNOS−/− mice. CYP reduced lung nitrotyrosine levels in both iNOS+/+ and iNOS−/− mice to uninfected-control levels as shown by immunohistochemical staining and enzyme-linked immunosorbent assay and inhibited mycoplasmal killing by iNOS+/+ mice in vivo. CYP inhibited the production of gamma interferon-inducible NOx by iNOS+/+ AMs in vitro but did not alter the number of iNOS-positive AMs, as detected by immunocytochemistry. In addition, AMs from CYP-treated iNOS+/+ mice had significantly decreased ability to kill mycoplasmas in vitro. These results demonstrate that reactive species generated by inflammatory cells as well as PMN myeloperoxidase are important contributors to nitrotyrosine formation during mycoplasmal infection and that treatment with CYP decreases NO⋅ production by AMs and inhibits mycoplasmal killing.
机译：我们先前曾报道，感染肺炎支原体的同基因C57BL / 6诱导型一氧化氮合酶-/-（iNOS-/-）小鼠比C57BL / 6 iNOS + / +对照具有更高的细菌数量和肺损伤评分，但肺硝基酪氨酸水平相似。本研究调查了炎症细胞在支原体感染过程中硝基酪氨酸形成中的作用。向iNOS + / +和iNOS-/-小鼠注射环磷酰胺（CYP），并接种107 CFU肺炎支原体。 CYP预处理对肺炎支原体感染的iNOS + / +和iNOS-/-小鼠的支气管肺泡灌洗液（BAL）内的多形核细胞（PMN）分别降低了88％和72％，全肺髓过氧化物酶水平分别降低了80％和78％ ，在感染后72小时，但并没有改变BAL中肺泡巨噬细胞（AM）的数量。 CYP处理还显着降低了感染的iNOS + / +小鼠的BAL和血浆中的硝酸盐和亚硝酸盐（NOx）水平，而CYP和支原体感染均未改变iNOS-/-小鼠的NOx。 CYP将iNOS + / +和iNOS-/-小鼠的肺硝基酪氨酸水平降低至未感染的对照水平（如免疫组织化学染色和酶联免疫吸附测定所示），并抑制了iNOS + / +小鼠体内的支原体杀伤作用。 CYP抑制了iNOS + / + AM在体外对γ干扰素诱导型NOx的产生，但并未改变免疫细胞化学检测到的iNOS阳性AM的数量。此外，CYP治疗的iNOS + / +小鼠的AMs在体外杀死支原体的能力明显降低。这些结果表明，炎症细胞以及PMN髓过氧化物酶产生的反应性物种是支原体感染期间硝化酪氨酸形成的重要贡献者，而CYP处理可减少AMs产生NO·并抑制支原体杀伤。

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