Bacterial Translocation and Host Immune Activation in Chronic Hepatitis C Infection

被引：15

作者：

Moon, Mi Sun ^{[1
,3
]}

Quinn, Gabriella ^{[1
]}

Townsend, Elizabeth C. ^{[1
]}

Ali, Rabab O. ^{[1
]}

Zhang, Grace Y. ^{[1
]}

Bradshaw, Alyson ^{[1
]}

Hill, Kareen ^{[1
]}

Guan, Hannah ^{[1
]}

Hamilton, Destanee ^{[1
]}

Kleiner, David E. ^{[2
]}

Koh, Christopher ^{[1
]}

Heller, Theo ^{[1
]}

机构：

[1] NIDDK, Translat Hepatol Sect, Liver Dis Branch, NIH, Bldg 10,Room 9B16,10 Ctr Dr MSC 1800, Bethesda, MD 20892 USA

[2] NCI, Lab Pathol, NIH, Bethesda, MD 20892 USA

[3] US FDA, Silver Spring, MD USA

来源：

OPEN FORUM INFECTIOUS DISEASES | 2019年 / 6卷 / 07期

关键词：

bacterial translocation; endotoxin; hepatitis C virus (HCV); macrophage activation; MACROPHAGE ACTIVATION;

D O I：

10.1093/ofid/ofz255

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Hepatitis C virus (HCV) infects 71 million individuals, and barriers to treatment remain. Bacterial translocation is a complication of chronic HCV infection, and this study evaluated circulating microbial components including lipopolysaccharide, peptidoglycan, and beta-D-glucan in addition to their pattern recognition receptors and degree of hepatic macrophage uptake. The findings suggest that regulation of serum peptidoglycan and beta-D-glucan differs from that of lipopolysaccharide. Additionally, macrophage activation in the liver may be better reflected by the degree of macrophage uptake than by circulating levels of microbial markers. These findings allow for a greater understanding of bacterial translocation and host immune activation during HCV infection.

引用

页数：5

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