title: 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.
authors.affiliation: Institute of Microbiology and Immunology, National Yang-Ming University, Taipei City, Taiwan; Infection and Immunity Research Center, National Yang-Ming University, Taipei City, Taiwan. Electronic address: cmleu@ym.edu.tw.
authors.forename: Chuen-Miin
authors.initials: CM
authors.lastname: Leu
authors.affiliation: Institute of Microbiology and Immunology, National Yang-Ming University, Taipei City, Taiwan.
authors.forename: Yong-Chen
authors.initials: YC
authors.lastname: Lu
authors.affiliation: Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei City, Taiwan.
authors.forename: Wei-Li
authors.initials: WL
authors.lastname: Peng
authors.affiliation: Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei City, Taiwan.
authors.forename: Hsin-Tzu
authors.initials: HT
authors.lastname: Chu
authors.affiliation: Department of Medical Research and Education, Taipei Veterans General Hospital, Taipei City, Taiwan; Department of Life Science, Tunghai University, Taichung City, Taiwan. Electronic address: cphu@thu.edu.tw.
authors.forename: Cheng-po
authors.initials: CP
authors.lastname: Hu
mesh_terms: D017209:Apoptosis / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018925:Chemokines / Q000096:biosynthesis; D002634:Chemotaxis, Leukocyte / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis; D006513:Hepatitis B e Antigens / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D011485:Protein Binding; D011994:Recombinant Proteins / Q000276:immunology / Q000378:metabolism; D016897:Respiratory Burst / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
chemical_list: D018925:Chemokines; D016207:Cytokines; D006513:Hepatitis B e Antigens; D011994:Recombinant Proteins
keywords: Chemokinesis; Hepatitis B virus e antigen; Innate immune response; Monocytes; Neutrophils; Respiratory burst