VDUP1 exacerbates bacteremic shock in mice infected with Pseudomonas aeruginosa

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dc.contributor.authorZ H Piao-
dc.contributor.authorM S Kim-
dc.contributor.authorM Jeong-
dc.contributor.authorSohyun Yun-
dc.contributor.authorS H Lee-
dc.contributor.authorH N Sun-
dc.contributor.authorHae Young Song-
dc.contributor.authorHyun Woo Suh-
dc.contributor.authorHaiyoung Jung-
dc.contributor.authorSuk Ran Yoon-
dc.contributor.authorTae-Don Kim-
dc.contributor.authorY H Lee-
dc.contributor.authorIn Pyo Choi-
dc.date.accessioned2017-04-19T09:35:58Z-
dc.date.available2017-04-19T09:35:58Z-
dc.date.issued2012-
dc.identifier.issn0008-8749-
dc.identifier.uri10.1016/j.cellimm.2012.11.003ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11107-
dc.description.abstractVitamin-D3 upregulated protein-1 (VDUP1) is a stress response protein. Pseudomonas aeruginosa (P. aeruginosa) infection is a leading cause of death. Mice infected with live P. aeruginosa exhibit significantly decreased VDUP1 expression. However, the function of VDUP1 during P. aeruginosa-induced mouse bacteremic shock is unknown. To address the function of VDUP1 in P. aeruginosa-infected mice, we constructed a bacteremic shock model wherein both wild-type and VDUP1-deficient mice were infected intra-peritoneally with live P. aeruginosa. We found that VDUP1-deficient mice were more resistant to P. aeruginosa-induced bacteremic shock than wild-type mice, as shown by the increased survival, accelerated bacterial clearance and suppression of cytokine overproduction of the VDUP1-deficient mice. VDUP1 promoted the recruitment of neutrophils into the peritoneal cavities of infected mice. VDUP1 impeded the phagocytosis of non-opsonized P. aeruginosa via phosphatidylinositide 3-kinase (PI3K) pathway in macrophages. P. aeruginosa infection induced the generation of reactive oxygen species (ROS), and the increased production of ROS by the peritoneal cells of VDUP1-deficient mice was advantageous in clearing the bacteria. Overall, VDUP1 aggravates bacteremic shock; thus, VDUP1 can be considered a target molecule for the inhibition of P. aeruginosa-induced bacteremic shock.-
dc.publisherElsevier-
dc.titleVDUP1 exacerbates bacteremic shock in mice infected with Pseudomonas aeruginosa-
dc.title.alternativeVDUP1 exacerbates bacteremic shock in mice infected with Pseudomonas aeruginosa-
dc.typeArticle-
dc.citation.titleCellular Immunology-
dc.citation.number1-
dc.citation.endPage9-
dc.citation.startPage1-
dc.citation.volume280-
dc.contributor.affiliatedAuthorSohyun Yun-
dc.contributor.affiliatedAuthorHae Young Song-
dc.contributor.affiliatedAuthorHyun Woo Suh-
dc.contributor.affiliatedAuthorHaiyoung Jung-
dc.contributor.affiliatedAuthorSuk Ran Yoon-
dc.contributor.affiliatedAuthorTae-Don Kim-
dc.contributor.affiliatedAuthorIn Pyo Choi-
dc.contributor.alternativeNamePiao-
dc.contributor.alternativeName김미선-
dc.contributor.alternativeName정미라-
dc.contributor.alternativeName윤소현-
dc.contributor.alternativeName이석형-
dc.contributor.alternativeNameSun-
dc.contributor.alternativeName송해영-
dc.contributor.alternativeName서현우-
dc.contributor.alternativeName정해용-
dc.contributor.alternativeName윤석란-
dc.contributor.alternativeName김태돈-
dc.contributor.alternativeName이영호-
dc.contributor.alternativeName최인표-
dc.identifier.bibliographicCitationCellular Immunology, vol. 280, no. 1, pp. 1-9-
dc.identifier.doi10.1016/j.cellimm.2012.11.003-
dc.subject.keywordBacteremic shock-
dc.subject.keywordP. aeruginosa-
dc.subject.keywordROS-
dc.subject.keywordVDUP1-
dc.subject.localBacteremic shock-
dc.subject.localP. aeruginosa-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localVDUP1-
dc.description.journalClassY-
Appears in Collections:
Aging Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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