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Infection of human macrophages with an endogenous tumour necrosis factor-alpha (TNF-alpha)-independent human immunodeficiency virus type 1 isolate is unresponsive to the TNF-alpha synthesis inhibitor RP 55778.用一种内源性肿瘤坏死因子-α(TNF-α)非依赖性1型人类免疫缺陷病毒分离株感染人类巨噬细胞,对TNF-α合成抑制剂RP 55778无反应。
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Cytokine-mediated induction of human immunodeficiency virus (HIV) expression and cell death in chronically infected U1 cells: do tumor necrosis factor alpha and gamma interferon selectively kill HIV-infected cells?细胞因子介导的慢性感染U1细胞中人免疫缺陷病毒(HIV)表达及细胞死亡:肿瘤坏死因子α和γ干扰素是否选择性杀伤HIV感染细胞?
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[Differential growth inhibition of mycobacteria by interferon-gamma-or tumor necrosis factor-alpha-treated murine peritoneal macrophages].[干扰素-γ或肿瘤坏死因子-α处理的小鼠腹腔巨噬细胞对分枝杆菌的差异生长抑制作用]
Kekkaku. 1996 Nov;71(11):607-14.
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The nature of extracellular iron influences iron acquisition by Mycobacterium tuberculosis residing within human macrophages.细胞外铁的性质会影响寄生于人类巨噬细胞内的结核分枝杆菌获取铁的过程。
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本文引用的文献

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Increased antimycobacterial immunity in interleukin-10-deficient mice.白细胞介素-10缺陷小鼠中抗分枝杆菌免疫力增强。
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Tuberculosis in patients with human immunodeficiency virus infection.人类免疫缺陷病毒感染患者的结核病
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Development of a rapid method for quantitative evaluation of Mycobacterium tuberculosis growth based on competitive polymerase chain reaction.
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Tumour necrosis factor (TNF) and TNF-related molecules in HIV-1+ individuals: relationship with in vitro Th1/Th2-type response.HIV-1阳性个体中的肿瘤坏死因子(TNF)及TNF相关分子:与体外Th1/Th2型反应的关系
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Enhanced interleukin-10 production in response to Mycobacterium avium products in mononuclear cells from patients with human immunodeficiency virus infection.人类免疫缺陷病毒感染患者单核细胞对鸟分枝杆菌产物反应中白细胞介素-10产生增强。
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Interleukin-10-induced HIV-1 expression is mediated by induction of both membrane-bound tumour necrosis factor (TNF)-alpha and TNF receptor type 1 in a promonocytic cell line.白细胞介素-10诱导的HIV-1表达是由前单核细胞系中膜结合肿瘤坏死因子(TNF)-α和1型TNF受体的诱导介导的。
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Effect of Mycobacterium tuberculosis on HIV replication. Role of immune activation.结核分枝杆菌对HIV复制的影响。免疫激活的作用。
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Functions of T-cell subsets and cytokines in mycobacterial infections.T细胞亚群和细胞因子在分枝杆菌感染中的作用。
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10
Evidence against a role for interleukin-10 in the regulation of growth of Mycobacterium avium in human monocytes.关于白细胞介素-10在调节人单核细胞中鸟分枝杆菌生长方面不起作用的证据。
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HIV-1感染的人类巨噬细胞中结核分枝杆菌生长增加:肿瘤坏死因子-α的作用

Increased Mycobacterium tuberculosis growth in HIV-1-infected human macrophages: role of tumour necrosis factor-alpha.

作者信息

Imperiali F G, Zaninoni A, La Maestra L, Tarsia P, Blasi F, Barcellini W

机构信息

Division of Hematology, University of Milan, IRCCS Ospedale Maggiore, Milan, Italy.

出版信息

Clin Exp Immunol. 2001 Mar;123(3):435-42. doi: 10.1046/j.1365-2249.2001.01481.x.

DOI:10.1046/j.1365-2249.2001.01481.x
PMID:11298131
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1906017/
Abstract

Synergism between Mycobacterium tuberculosis (M. tuberculosis) and HIV-1 infections was demonstrated in several in vitro models and clinical studies. Here, we investigated their reciprocal effects on growth in chronically HIV-1-infected promonocytic U1 cells and in acutely infected monocyte-derived macrophages (MDM). Phagocytosis of M. tuberculosis induced HIV-1 expression in U1 cells, together with increased TNF-alpha production. M. tuberculosis growth, evaluated by competitive PCR, was greater in HIV-1-infected MDM compared to uninfected cells. M. tuberculosis phagocytosis induced greater TNF-alpha and IL-10 production in HIV-1-infected MDM than in uninfected cells. In uninfected MDM, addition of TNF-alpha and IFN-gamma decreased, whereas IL-10 increased M. tuberculosis growth. On the contrary, in HIV-1-infected MDM, addition of TNF-alpha and IFN-gamma increased, whereas IL-10 has no effect on M. tuberculosis growth. TNF-alpha seems to play a pivotal role in the enhanced M. tuberculosis growth observed in HIV-1-infected MDM, being unable to exert its physiological antimycobacterial activity. Here, for the first time we demonstrated an enhanced M. tuberculosis growth in HIV-1-infected MDM, in line with the observed clinical synergism between the two infections.

摘要

结核分枝杆菌(M. tuberculosis)与HIV-1感染之间的协同作用已在多个体外模型和临床研究中得到证实。在此,我们研究了它们对慢性HIV-1感染的前单核细胞U1细胞和急性感染的单核细胞衍生巨噬细胞(MDM)生长的相互影响。结核分枝杆菌的吞噬作用诱导了U1细胞中HIV-1的表达,同时TNF-α的产生增加。通过竞争性PCR评估,HIV-1感染的MDM中结核分枝杆菌的生长比未感染细胞中的更大。结核分枝杆菌的吞噬作用在HIV-1感染的MDM中比在未感染细胞中诱导产生更多的TNF-α和IL-10。在未感染的MDM中,添加TNF-α和IFN-γ会降低结核分枝杆菌的生长,而IL-10则会增加其生长。相反,在HIV-1感染的MDM中,添加TNF-α和IFN-γ会增加结核分枝杆菌的生长,而IL-10对其生长没有影响。TNF-α似乎在HIV-1感染的MDM中观察到的结核分枝杆菌生长增强中起关键作用,无法发挥其生理抗分枝杆菌活性。在此,我们首次证明了HIV-1感染的MDM中结核分枝杆菌生长增强,这与两种感染之间观察到的临床协同作用一致。