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The hepatitis B virus e antigen suppresses the respiratory burst and mobility of human monocytes and neutrophils.

Abstract：

:The Hepatitis B virus (HBV) e antigen (HBeAg) is a secretory, non-structural protein, and associated with persistent infection of HBV. Previous studies indicate that HBeAg is able to regulate T cell-mediated responses, however, the interaction between HBeAg and the innate immune system is poorly understood. In this study, we demonstrated that recombinant HBeAg (rHBe) bound to human peripheral blood monocytes, neutrophils, and B lymphocytes but not to T lymphocytes. We focused on investigating the effects of HBeAg on monocytes and neutrophils and found that rHBe decreased the respiratory burst in both types of cells. Furthermore, we observed that cell migration in monocytes and neutrophils was suppressed by rHBe in a transwell assay. The attenuation of rHBe was not caused by a general cytotoxic effect because rHBe treatment stimulated low levels of cytokine and chemokine production by monocytes and it promoted neutrophil survival. Since the recruitment of monocytes and neutrophils to the infected site is crucial for the initiation of inflammation, HBeAg may modulate innate immune responses by diminishing the respiratory burst and migration of monocytes and neutrophils, which might interfere with the subsequent innate and adaptive immune responses against HBV, leading to the establishment of chronic infection.

journal_name

Immunobiology

journal_title

Immunobiology

authors

Leu CM,Lu YC,Peng WL,Chu HT,Hu CP

doi

10.1016/j.imbio.2014.07.008

subject

Has Abstract

pub_date

2014-11-01 00:00:00

pages

880-7

issue

11

eissn

0171-2985

issn

1878-3279

pii

S0171-2985(14)00121-1

journal_volume

219

pub_type

杂志文章

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