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微小脲原体在药理学免疫受损小鼠模型中可导致高氨血症。

Ureaplasma parvum causes hyperammonemia in a pharmacologically immunocompromised murine model.

作者信息

Wang X, Greenwood-Quaintance K E, Karau M J, Block D R, Mandrekar J N, Cunningham S A, Mallea J M, Patel R

机构信息

Division of Clinical Microbiology, Department of Laboratory Medicine and Pathology, Mayo Clinic, 200 First St S.W., Rochester, MN, 55905, USA.

Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

出版信息

Eur J Clin Microbiol Infect Dis. 2017 Mar;36(3):517-522. doi: 10.1007/s10096-016-2827-1. Epub 2016 Oct 28.

Abstract

A relationship between hyperammonemia and Ureaplasma infection has been shown in lung transplant recipients. We have demonstrated that Ureaplasma urealyticum causes hyperammonemia in a novel immunocompromised murine model. Herein, we determined whether Ureaplasma parvum can do the same. Male C3H mice were given mycophenolate mofetil, tacrolimus, and prednisone for 7 days, and then challenged with U. parvum intratracheally (IT) and/or intraperitoneally (IP), while continuing immunosuppression over 6 days. Plasma ammonia concentrations were determined and compared using Wilcoxon rank-sum tests. Plasma ammonia concentrations of immunosuppressed mice challenged IT/IP with spent broth (median, 188 μmol/L; range, 102-340 μmol/L) were similar to those of normal (median, 226 μmol/L; range, 154-284 μmol/L, p > 0.05), uninfected immunosuppressed (median, 231 μmol/L; range, 122-340 μmol/L, p > 0.05), and U. parvum IT/IP challenged immunocompetent (median, 226 μmol/L; range, 130-330 μmol/L, p > 0.05) mice. Immunosuppressed mice challenged with U. parvum IT/IP (median 343 μmol/L; range 136-1,000 μmol/L) or IP (median 307 μmol/L; range 132-692 μmol/L) had higher plasma ammonia concentrations than those challenged IT/IP with spent broth (p < 0.001). U. parvum can cause hyperammonemia in pharmacologically immunocompromised mice.

摘要

肺移植受者中已显示高氨血症与解脲脲原体感染之间存在关联。我们已证明解脲脲原体在一种新型免疫受损小鼠模型中可导致高氨血症。在此,我们确定微小脲原体是否也能如此。雄性C3H小鼠接受霉酚酸酯、他克莫司和泼尼松治疗7天,然后经气管内(IT)和/或腹腔内(IP)接种微小脲原体,同时在6天内持续进行免疫抑制。使用Wilcoxon秩和检验测定并比较血浆氨浓度。经IT/IP接种用过的肉汤的免疫抑制小鼠的血浆氨浓度(中位数,188μmol/L;范围,102 - 340μmol/L)与正常小鼠(中位数,226μmol/L;范围,154 - 284μmol/L,p>0.05)、未感染的免疫抑制小鼠(中位数,231μmol/L;范围,122 - 340μmol/L,p>0.05)以及经IT/IP接种微小脲原体的免疫 competent(中位数,226μmol/L;范围,130 - 330μmol/L,p>0.05)小鼠相似。经IT/IP(中位数343μmol/L;范围136 - 1000μmol/L)或IP(中位数307μmol/L;范围132 - 692μmol/L)接种微小脲原体的免疫抑制小鼠的血浆氨浓度高于经IT/IP接种用过的肉汤的小鼠(p<0.001)。微小脲原体可在药物诱导免疫受损的小鼠中导致高氨血症。

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