4.2 Article Proceedings Paper

Traumatic brain injury-induced alterations in peripheral immunity

期刊

JOURNAL OF TRAUMA AND ACUTE CARE SURGERY
卷 75, 期 5, 页码 780-788

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/TA.0b013e318299616a

关键词

Traumatic brain injury; immunosuppression; peripheral immunity; innate immunity; mice

资金

  1. NHLBI NIH HHS [P01 HL108795, HL108795] Funding Source: Medline
  2. NIAID NIH HHS [R21 AI092490, AI092490] Funding Source: Medline
  3. NIAMS NIH HHS [AR054796, R01 AR050250, R01 AR054796, AR050250] Funding Source: Medline

向作者/读者索取更多资源

BACKGROUND: The complex alterations that occur in peripheral immunity after traumatic brain injury (TBI) have been poorly characterized to date. The purpose of this study was to determine the temporal changes in the peripheral immune response after TBI in a murine model of closed head injury. METHODS: C57Bl/6 mice underwent closed head injury via a weight drop technique (n = 5) versus sham injury (n = 3) per time point. Blood, spleen, and thymus were collected, and immune phenotype, cytokine expression, and antibody production were determined via flow cytometry and multiplex immunoassays at 1, 3, 7, 14, 30, and 60 days after injury. RESULTS: TBI results in acute and chronic changes in both the innate and adaptive immune response. TBI resulted in a striking loss of thymocytes as early as 3 days after injury (2.1 x 10(7) TBI vs. 5.6 x 10(7) sham, p = 0.001). Similarly, blood monocyte counts were markedly diminished as early as 24 hours after TBI (372 per deciliter TBI vs. 1359 per deciliter sham, p = 0.002) and remained suppressed throughout the first month after injury. At 60 days after injury, monocytes were polarized toward an anti-inflammatory (M2) phenotype. TBI also resulted in diminished interleukin 12 expression from Day 14 after injury throughout the remainder of the observation period. CONCLUSION: TBI results in temporal changes in both the peripheral and the central immune systems culminating in an overall immune suppressed phenotype and anti-inflammatory milieu. (J Trauma Acute Care Surg. 2013;75:780-788. Copyright (C) 2013 by Lippincott Williams & Wilkins)

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