Anticipation of organ dysfunction by immmunological monitoring in severe trauma and burns

Research Project

Project/Area Number	24592748
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Emergency medicine
Research Institution	Keio University
Principal Investigator	Sekine Kazuhiko 慶應義塾大学, 医学部, 講師 (90296715)
Project Period (FY)	2012-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000) Fiscal Year 2014: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000) Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000) Fiscal Year 2012: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Keywords	免疫 / 侵襲 / 臓器不全 / 白血球 / フェノタイプ解析 / 外傷 / 熱傷 / アレイ / 表面抗原 / 免疫不全 / 易感染性 / 白血球フェノタイプ
Outline of Final Research Achievements	Sepsis-induced organ dysfunction (SIOD) has been considered to be involved in leukocyte phenotypic changes in severely injured and burned patients. Our question is whether SIOD can be predicted by leukocyte immunophenotyping or not in these trauma or burned patients, using a new array method we developed. Among 16 patients with trauma/burns and 5 healthy volunteers, we analyzed the leukocyte phenotypes including CD4/8/11c/16b/25/36/66b/123/127/161, Toll like receptor (TLR)-2/4, CC-Chemokine receptor (CCR)-2/4/5, CXC-Chemokine receptor (CXCR)-3, and CRTh2. In burned patients, phenotypes were lower not only in CCR5 and CXCR3 than those in both trauma and healthy subjects, and also in CD68 and CD123 than those in trauma, whereas phenotypes in Th1 (CCR5, CXCR3) and monocytes /dendritic cells (CCR2, CD11c) were increased. Based on these results, re-increase of Th1 phenotypes may predict infectious complications or organ dysfunction after burn insults.