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一氧化氮未参与肺泡巨噬细胞杀灭烟曲霉分生孢子的过程。

Lack of involvement of nitric oxide in killing of Aspergillus fumigatus conidia by pulmonary alveolar macrophages.

作者信息

Michaliszyn E, Sénéchal S, Martel P, de Repentigny L

机构信息

Department of Microbiology and Immunology, Faculty of Medicine, University of Montreal, Quebec, Canada.

出版信息

Infect Immun. 1995 May;63(5):2075-8. doi: 10.1128/iai.63.5.2075-2078.1995.

DOI:10.1128/iai.63.5.2075-2078.1995
PMID:7729922
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC173267/
Abstract

Nitric oxide is an important antimicrobial mechanism of phagocytes from mice and rats, but in the case of human phagocytes, secretion is still controversial. We investigated whether nitric oxide is involved in the killing of Aspergillus fumigatus conidia by human or murine pulmonary alveolar macrophages. Stimulation of the macrophages with gamma interferon and Escherichia coli lipopolysaccharide had no effect on fungicidal activity against conidia in vitro, with or without the addition of tetrahydrobiopterin. Killing of conidia (means +/- standard deviations) by murine or human alveolar macrophages, before and after stimulation, was 44% +/- 13% and 49% +/- 12% (P = 0.34) and 24% +/- 5% and 29% +/- 10% (P = 0.20), respectively. Fungicidal activity was unaltered in the presence of the competitive inhibitor NG-monomethyl L-arginine, and nitrite was undetectable in cell supernatants. Peritoneal macrophages from B6C3F1 mice produced 18 mumol of nitrite per 10(6) cells in 18 h. In conclusion, nitric oxide does not appear to be involved in the fungicidal activity of murine or human alveolar macrophages against A. fumigatus conidia.

摘要

一氧化氮是小鼠和大鼠吞噬细胞的一种重要抗菌机制,但对于人类吞噬细胞而言,其分泌情况仍存在争议。我们研究了一氧化氮是否参与人类或鼠类肺泡巨噬细胞对烟曲霉分生孢子的杀伤作用。用γ干扰素和大肠杆菌脂多糖刺激巨噬细胞,无论是否添加四氢生物蝶呤,对体外分生孢子的杀真菌活性均无影响。刺激前后,鼠类或人类肺泡巨噬细胞对分生孢子的杀伤率(平均值±标准差)分别为44%±13%和49%±12%(P = 0.34),以及24%±5%和29%±10%(P = 0.20)。在存在竞争性抑制剂NG-单甲基L-精氨酸的情况下,杀真菌活性未改变,且在细胞上清液中未检测到亚硝酸盐。B6C3F1小鼠的腹腔巨噬细胞在18小时内每10(6)个细胞产生18微摩尔亚硝酸盐。总之,一氧化氮似乎不参与鼠类或人类肺泡巨噬细胞对烟曲霉分生孢子的杀真菌活性。

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