| pubmed-article:18838943 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C0376515 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C1533157 | lld:lifeskim |
| pubmed-article:18838943 | lifeskim:mentions | umls-concept:C0333668 | lld:lifeskim |
| pubmed-article:18838943 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18838943 | pubmed:dateCreated | 2009-3-18 | lld:pubmed |
| pubmed-article:18838943 | pubmed:abstractText | This study examined the fate of dendritic cells (DCs) and macrophages (M Phi) in vivo in a murine model of sepsis. Wild-type, knockout, and transgenic mice were used to examine the role of Bcl-2 family members on the regulation of splenic DCs and M Phi survival. Bim knockout (Bim) mice and mice overexpressing Bcl-2 in selected hematopoietic cells were used: (a) overexpression of Bcl-2 in all hematopoietic cells using a vav promoter (Vav-Bcl-2) and (b) overexpression of Bcl-2 in all Major histocompatibility complex (MHC) class I cells (H-2K-Bcl-2). Mice underwent sham surgery or cecal ligation and puncture, and absolute numbers of splenic DCs and M Phi were determined. Importantly, two distinct M Phi populations, that is, well-differentiated "mature" M Phi population and a less differentiated "immature," "monocyte-like" (IM Phi) population were identified that demonstrated differential susceptibility to apoptosis. In wild-type mice, sepsis induced a 64% +/- 7% and a 77% +/- 3% decrease in absolute cell numbers of splenic DCs and IM Phi, respectively (n = 7, P < 0.05). Mature M Phi were not depleted in sepsis. No significant cell depletion was evident in Vav-Bcl-2, H-2K-Bcl-2, or Bim mice. We conclude that sepsis induces a major depletion of developing M Phi as well as DCs, and this depletion may be an important mechanism of immune suppression in sepsis. | lld:pubmed |
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| pubmed-article:18838943 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18838943 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18838943 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18838943 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18838943 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18838943 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18838943 | pubmed:issn | 1540-0514 | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:HotchkissRich... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:ChangKatherin... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:McDonoughJacq... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:PerlmanHarris... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:McDunnJonatha... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:UnsingerJacqu... | lld:pubmed |
| pubmed-article:18838943 | pubmed:author | pubmed-author:Peck-PalmerOc... | lld:pubmed |
| pubmed-article:18838943 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18838943 | pubmed:volume | 31 | lld:pubmed |
| pubmed-article:18838943 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18838943 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18838943 | pubmed:pagination | 359-66 | lld:pubmed |
| pubmed-article:18838943 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:meshHeading | pubmed-meshheading:18838943... | lld:pubmed |
| pubmed-article:18838943 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:18838943 | pubmed:articleTitle | Modulation of the Bcl-2 family blocks sepsis-induced depletion of dendritic cells and macrophages. | lld:pubmed |
| pubmed-article:18838943 | pubmed:affiliation | Department of Anesthesiology, Washington University School of Medicine, St Louis, Missouri, USA. | lld:pubmed |
| pubmed-article:18838943 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18838943 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18838943 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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