2008
DOI: 10.1016/j.jinf.2007.10.008
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Dengue virus infection induces passive release of high mobility group box 1 protein by epithelial cells

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Cited by 41 publications
(30 citation statements)
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“…2A) support the idea that passively released HMGB1 could contribute to influenza-induced mortality, as has been postulated (26). Local production of HMGB1 via passive release is possible during influenza infections, because other viruses are known to induce HMGB1 leak from infected cells (27)(28)(29). Furthermore, our results using ethyl pyruvate to reduce active secretion of HMGB1 support the notion that active secretion of HMGB1 might occur too late in influenza virus infections to significantly affect mortality (Fig.…”
Section: Discussionsupporting
confidence: 86%
“…2A) support the idea that passively released HMGB1 could contribute to influenza-induced mortality, as has been postulated (26). Local production of HMGB1 via passive release is possible during influenza infections, because other viruses are known to induce HMGB1 leak from infected cells (27)(28)(29). Furthermore, our results using ethyl pyruvate to reduce active secretion of HMGB1 support the notion that active secretion of HMGB1 might occur too late in influenza virus infections to significantly affect mortality (Fig.…”
Section: Discussionsupporting
confidence: 86%
“…HMGB1 contains three conserved redox-sensitive cysteines (C23, C45, and C106); modification of these cysteines determines the bioactivity of extracellular HMGB1 [18]. HMGB1 can be passively released by necrotic cells, cells infected by viruses [19][20][21][22] or mycobacteria [23,24], and actively released by innate immune cells in respond to endogenous host stimuli or exogenous bacterial products [25], and serves as a signaling molecule involve in acute and chronic inflammatory injury by binding to the receptor for advanced glycation end-products (RAGE) or Toll-like receptors (TLR2, 4 and 9), which results in the activation of pro-inflammatory pathways and enhanced inflammatory injury [15]. Therefore, the anti-inflammatory strategies based on targeting HMGB1 is of significant experimental and clinical interests.…”
Section: Introductionmentioning
confidence: 99%
“…8 The involvement of HMGB1 in DENV infection was first observed in DENV-infected epithelial cells undergoing necrosis, which passively released this molecule into the extracellular milieu. 9 Another report showed that DENV-infected dendritic cells actively translocate HMGB1 to the cytoplasm or even secrete it. 10 In our previous study, we demonstrated that circulating levels of HMGB1 in serum of DENV-infected patients were significantly increased, and the highest levels occurred during the first days after appearance of symptoms and in patients with a secondary infection.…”
mentioning
confidence: 99%
“…The quantitation of cytokines or endogenous proteins is uncommon because they are not specific for DENV infection, they may vary significantly in each patient, and their highest levels occur early in the infection, which makes them difficult to measure. It was observed that the pro-inflammatory cytokine HMGB1 is involved in DENV infection 9,10 and is detected at increased levels in serum samples from DENV-infected patients. 11 In contrast to other cytokines, HMGB1 is described as a late mediator of sepsis in comparison with the classical mediators, including tumor necrosis factor and interleukin 1.…”
mentioning
confidence: 99%