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 p...

Full description

Saved in:
Bibliographic Details
Published in:Immunobiology (1979) 2014-11, Vol.219 (11), p.880-887
Main Authors: Leu, Chuen-Miin, Lu, Yong-Chen, Peng, Wei-Li, Chu, Hsin-Tzu, Hu, Cheng-po
Format: Article
Language:English
Subjects:
Advanced Basic Science
Allergy and Immunology
Apoptosis - immunology
B-Lymphocytes - immunology
B-Lymphocytes - metabolism
Chemokines - biosynthesis
Chemokinesis
Chemotaxis, Leukocyte - immunology
Cytokines - biosynthesis
Hepatitis B e Antigens - immunology
Hepatitis B e Antigens - metabolism
Hepatitis B virus
Hepatitis B virus e antigen
Humans
Innate immune response
Monocytes
Monocytes - immunology
Monocytes - metabolism
Neutrophils
Neutrophils - immunology
Neutrophils - metabolism
Protein Binding
Recombinant Proteins - immunology
Recombinant Proteins - metabolism
Respiratory burst
Respiratory Burst - immunology
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0171-2985
1878-3279
DOI:10.1016/j.imbio.2014.07.008