2019
DOI: 10.1016/j.cyto.2018.06.002
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Porcine reproductive and respiratory syndrome virus induces concurrent elevation of High Mobility Group Box-1 protein and pro-inflammatory cytokines in experimentally infected piglets

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Cited by 20 publications
(15 citation statements)
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“…Lung cell damage caused by IAV infection and inflammation releases a large amount of HMGB-1 [11,65]. As a kind of DAMP, high level of HMGB-1 expression in lung leads to continuous activation of TLR4 signaling pathway and stimulates the inflammatory cells to continuously release cytokines, chemokines, as well as inducible nitric oxide, which accumulate in the injured lung tissue and further aggravate the tissue damage [66,67].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Lung cell damage caused by IAV infection and inflammation releases a large amount of HMGB-1 [11,65]. As a kind of DAMP, high level of HMGB-1 expression in lung leads to continuous activation of TLR4 signaling pathway and stimulates the inflammatory cells to continuously release cytokines, chemokines, as well as inducible nitric oxide, which accumulate in the injured lung tissue and further aggravate the tissue damage [66,67].…”
Section: Discussionmentioning
confidence: 99%
“…When the host is infected, the virus can induce a series of signaling cascades to their own benefit, such as toll-like receptors (TLRs) and other signaling pathways [10]. As we all know, pathogen-associated molecular pattern (PAMP), as well as damage-associated molecular pattern (DAMP) activate antigen-presenting cells through TLRs to initiate immune responses [11]. DAMPs such as high mobility group box-1 protein (HMGB-1) are released early from the infected host cells in the extracellular medium in response to viral stimuli.…”
Section: Introductionmentioning
confidence: 99%
“…Lung cell damage caused by IAV infection and in ammation releases a large amount of HMGB-1 [11,65]. As a kind of DAMP, high level of HMGB-1 expression in lung leads to continuous activation of TLR4 signaling pathway and stimulates the in ammatory cells to continuously release cytokines, chemokines, as well as inducible nitric oxide, which accumulate in the injured lung tissue and further aggravate the tissue damage [66,67].…”
Section: Discussionmentioning
confidence: 99%
“…When the host is infected, the virus can induce a series of signaling cascades to their own bene t, such as toll-like receptors (TLRs) and other signaling pathways [10]. As we all know, pathogen-associated molecular pattern (PAMP), as well as damage-associated molecular pattern (DAMP) activate antigen-presenting cells through TLRs to initiate immune responses [11]. DAMPs such as high mobility group box-1 protein (HMGB-1) are released early from the infected host cells in the extracellular medium in response to viral stimuli.…”
Section: Introductionmentioning
confidence: 99%
“…Since its first occurrence in 1987 in North America and 1991 in Europe, the disease has spread to Southeast Asian countries [16] and was introduced to India in 2013 in Mizoram [29]. The emergence of highly pathogenic strain and its rapid spread in Asian countries become a major concern in pig husbandry practice in this region as diseased animals exhibit severe respiratory distress, pneumonia, and a series of reproductive disorders in sows, like late-term abortion, premature farrowing, an increased number of stillborn piglets including high mortality by highly pathogenic strains [1][2][3][32][33][34]. The disease is caused by Betaarterivirus suid 1 (European type) and Betaarterivirus suid 2 (North American type) of the subgenus Eurpobartevirus and Ampobartevirus respectively under the genus Betaarterivirus of the subfamily Variarterivirinae of the family Arteriviridae in the order Nidovirales.…”
Section: Introductionmentioning
confidence: 99%