Dengue Virus Infection Mediates HMGB1 Release from Monocytes Involving PCAF Acetylase Complex and Induces Vascular Leakage in Endothelial Cells

Autor: Ling Min Lee, Yew Fai Ivan Leong, Justin Jang Hann Chu, Siew Pei Ong, Mah Lee Ng
Rok vydání: 2012
Předmět:
Viral Diseases
medicine.medical_treatment
Cell
lcsh:Medicine
Vascular permeability
Dengue virus
medicine.disease_cause
Monocytes
Dengue
Multiplicity of infection
p300-CBP Transcription Factors
HMGB1 Protein
lcsh:Science
Fluorescent Antibody Technique
Indirect
Multidisciplinary
Acetylation
Innate Immunity
Host-Pathogen Interaction
Infectious Diseases
Cytokine
medicine.anatomical_structure
Cytokines
Medicine
Electrophoresis
Polyacrylamide Gel
Research Article
Mechanisms of Resistance and Susceptibility
Blotting
Western
Immunology
chemical and pharmacologic phenomena
Biology
Microbiology
Capsid
Virology
medicine
Humans
Inflammation
lcsh:R
Host Cells
Immunity
Molecular biology
Cell culture
Cytoplasm
Immune System
Virulence Factors and Mechanisms
lcsh:Q
Endothelium
Vascular
K562 Cells
Viral Transmission and Infection
K562 cells
Zdroj: PLoS ONE
PLoS ONE, Vol 7, Iss 7, p e41932 (2012)
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0041932
Popis: High mobility group box 1 (HMGB1) protein is released from cells as a pro-inflammatory cytokine in response to an injury or infection. During dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS), a number of pro-inflammatory cytokines are released, contributing to disease pathogenesis. In this study, the release of HMGB1 from human myelogenous leukemia cell line K562 and primary peripheral blood monocytes (PBM) cells was examined during dengue virus (DV)-infection. HMGB1 was shown to translocate from cell nuclei to the cytoplasm in both K562- and PBM-infected cells. The translocation of HMGB1 from the nucleus to the cytoplasm was shown to be mediated by the host cell p300/CBP-associated factor (PCAF) acetylase complex in K562 cells. In addition, DV capsid protein was observed to be the putative viral protein in actuating HMGB1 migration from the nucleus to cytoplasm through the involvement of PCAF acetylase. HMGB1 was released from DV-infected K562 cells into the extracellular milieu in a multiplicity of infection (M.O.I.)-independent manner and its release can be inhibited by the addition of 1-5 mM of ethyl pyruvate (EP) in a dose-dependent manner. Application of DV-infected K562 cell culture supernatants to primary endothelial cells induced vascular permeability. In contrast, supernatants from DV-infected K562 cells treated with EP or HMGB1 neutralizing antibody were observed to maintain the structural integrity of the vascular barrier.
Databáze: OpenAIRE
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