Nitric Oxide Production in Peritoneal Macrophages from Peritoneal Dialysis Patients with Bacterial Peritonitis
Nitric Oxide Production in Peritoneal Macrophages from Peritoneal Dialysis Patients with Bacterial Peritonitis
复制标题
腹膜透析细菌性腹膜炎患者腹膜巨噬细胞中一氧化氮的产生
DOI：
--
复制
发表时间：
1999
影响因子：
2.8
通讯作者：
B. Grabensee
中科院分区：
文献类型：
--
作者：
J. Plum;Maryam Mirza Tabatabaei;M. R. Lordnejad;Olga Pipinika;P. Razeghi;Chumnei Huang;J. Meyer;B. Grabensee
一氧化氮（NO）是由多种细胞产生的，它是许多生物过程中的重要介质，包括巨噬细胞介导的细胞宿主防御。腹膜透析（PD）治疗期间腹膜炎中NO产生的相关性和数量尚不清楚。我们研究了从健康PD患者或患有腹膜炎的PD患者分离的人腹膜巨噬细胞（PMΦ）是否表现出不同的自发或脂多糖（LPS）/干扰素γ（IFN-γ）诱导的NO产生（LPS，1 ng/mL 10 μ g/mL; IFN-γ，10 1000 μ g/mL;孵育6 - 48小时;通过Griess试剂测量）。结果与从血沉棕黄层分离的人血单核细胞（HBM）进行了比较。逆转录聚合酶链反应（RT-PCR）检测PMΦ中诱导型一氧化氮合成酶（iNOS）mRNA的表达。此外，在体内测量血浆（P）和腹膜透析液流出物（D）的亚硝酸盐浓度。与无感染患者相比，腹膜炎患者亚硝酸盐浓度的透析液与血浆比率（DIP）是相反的（腹膜炎DIP = 1.3，非腹膜炎DIP = 0.4; p < 0.01）。腹膜炎患者的PMΦ产生的NO量高于无感染患者的PM Φ（0.040 ± 0.044 nmol/μ g细胞蛋白vs 0.018 ± 0.015 nmol/μ g细胞蛋白，p < 0.05）。用LPS和IFN-γ（分别为1 ng/mL、250 μ L）刺激不能进一步促进NO的释放。然而，在体外刺激期间，来自无感染患者的PMΦ中的NO产生增加（0.044 ± 0.031 nmol/μ g细胞蛋白对0.018± 0.015 nmol/μ g细胞蛋白，p < 0.01）。RT-PCR结果显示诱导型一氧化氮合酶mRNA表达增加。来自健康供体的血液单核细胞在细胞因子刺激期间也增加NO释放（0.032± 0.015 nmol/微克细胞蛋白对0.019 ± 0.009 nmol/微克细胞蛋白，p < 0.05）。我们的研究结果表明，在细菌性腹膜炎的情况下，大量的NO释放腹膜内。PMΦ代表NO产生的位点，尽管在体外释放的绝对量仅为中等。LPSIFN-y在体外可诱导PMΦ和HBM产生NO。
Nitric oxide (NO) is produced by various cell types, and it is an important mediator in many biological processes, including macrophage-mediated cellular host defense. The relevance and amount of NO production in peritonitis during peritoneal dialysis (PD) treatment is still not clear. We studied whether human peritoneal macrophages (PMΦ) isolated from healthy PD patients or PD patients with peritonitis showed different spontaneous or lipo-polysaccharide (LPS)linterferon gamma (IFN-y) -induced NO production (LPS, 1 nglmL 10 μglmL; IFN-y, 101000 UlmL; incubation between 6 -48 hours; measured by Griess reagent). Results were compared with human blood monocytes (HBM) isolated from buffy coats. Inducible nitric oxide synthetase (iNOS) mRNA expression was looked for in PMΦ by reverse transcriptase polymerase chain reaction (RT-PCR). Furthermore, plasma (P) and peritoneal dialysate effluent (D) nitrite concentrations were measured in vivo. The dialysate-to-plasma ratio (DIP) of nitrite concentration was inverse in the case of peritonitis compared to infection-free patients (peritonitis DIP = 1.3, non peritonitis DIP = 0.4; p < 0.01). PMΦ from peritonitis patients produced higher amounts of NO than did those from infection-free patients (0.040 ± 0.044 nmol per microgram cell protein versus 0.018 ± 0.015 nmol per microgram cell protein, p < 0.05). NO release could not be further enhanced by stimulation with LPS plus IFN-y (1 ng/mL, 250 UlmL, respectively). However, NO production in PMΦ from infection-free patients increased during in vitro stimulation (0.044 ± 0.031 nmol per microgram cell protein versus 0.018± 0.015 nmol per microgram cell protein, p < 0.01). An increase of iNOS mRNA expression could be demonstrated by RT-PCR. Blood monocytes from healthy donors also increased NO release during cytokine stimulation (0.032± 0.015 nmol per microgram cell protein versus 0.019 ± 0.009 nmol per microgram cell protein, p < 0.05). Our results indicate that significant amounts of NO are released intraperitoneally in the case of bacterial peritonitis. PMΦ represent a site of NO production, though the absolute amounts released in vitro are only moderate. NO production can be induced in PMΦ and HBM by LPSIIFN-y stimulation in vitro.
登录
查看更多内容
影响因子：
20.3
作者：
J. Weinberg;M. Misukonis;P. Shami;S. Mason;D. Sauls;W. Dittman;ER Wood;GK Smith;B. McDonald;K. Bachus
通讯作者：
J. Weinberg;M. Misukonis;P. Shami;S. Mason;D. Sauls;W. Dittman;ER Wood;GK Smith;B. McDonald;K. Bachus
影响因子：
20.3
作者：
C. Dinarello
通讯作者：
C. Dinarello
内毒素、白介素-1 和肿瘤坏死因子导致毛细血管后微静脉中中性粒细胞依赖性微血管渗漏。
DOI：
--
发表时间：
1992
期刊：
The American journal of pathology
影响因子：
--
作者：
Yi,ES;Ulich,TR
通讯作者：
Ulich,TR
P-和L-选择素在大鼠肠系膜微循环中内毒素诱导的白细胞-内皮相互作用中介导不同但重叠的功能。
DOI：
--
发表时间：
1997
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Davenpeck,KL;Steeber,DA;Tedder,TF;Bochner,BS
通讯作者：
Bochner,BS
阻断疾病中的 IL-1。
影响因子：
3
作者：
Dinarello,CA
通讯作者：
Dinarello,CA