Document Detail


Radiation combined with thermal injury induces immature myeloid cells.
MedLine Citation:
PMID:  23042190     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The continued development of nuclear weapons and the potential for thermonuclear injury necessitates the further understanding of the immune consequences after radiation combined with injury (RCI). We hypothesized that sublethal ionization radiation exposure combined with a full-thickness thermal injury would result in the production of immature myeloid cells. Mice underwent either a full-thickness contact burn of 20% total body surface area or sham procedure followed by a single whole-body dose of 5-Gy radiation. Serum, spleen, and peripheral lymph nodes were harvested at 3 and 14 days after injury. Flow cytometry was performed to identify and characterize adaptive and innate cell compartments. Elevated proinflammatory and anti-inflammatory serum cytokines and profound leukopenia were observed after RCI. A population of cells with dual expression of the cell surface markers Gr-1 and CD11b were identified in all experimental groups, but were significantly elevated after burn alone and RCI at 14 days after injury. In contrast to the T-cell-suppressive nature of myeloid-derived suppressor cells found after trauma and sepsis, myeloid cells after RCI augmented T-cell proliferation and were associated with a weak but significant increase in interferon γ and a decrease in interleukin 10. This is consistent with previous work in burn injury indicating that a myeloid-derived suppressor cell-like population increases innate immunity. Radiation combined injury results in the increase in distinct populations of Gr-1CD11b cells within the secondary lymphoid organs, and we propose these immature inflammatory myeloid cells provide innate immunity to the severely injured and immunocompromised host.
Authors:
April Elizabeth Mendoza; Crystal Judith Neely; Anthony G Charles; Laurel Briane Kartchner; Willie June Brickey; Amal Lina Khoury; Gregory D Sempowski; Jenny P Y Ting; Bruce A Cairns; Robert Maile
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  38     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-18     Completed Date:  2013-03-11     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  532-42     Citation Subset:  IM    
Affiliation:
Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, USA. amendo@lsuhsc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Burns / blood,  immunology*,  pathology
Cytokines / blood,  immunology
Female
Flow Cytometry
Gamma Rays / adverse effects*
Leukopenia / blood,  etiology,  immunology,  pathology
Lymph Nodes / immunology,  metabolism,  pathology
Mice
Myeloid Cells / immunology*,  metabolism,  pathology
Nuclear Weapons
Radiation Injuries, Experimental / blood,  immunology*,  pathology
T-Lymphocytes / immunology,  metabolism,  pathology
Grant Support
ID/Acronym/Agency:
R01 GM076250/GM/NIGMS NIH HHS; R0GM076250-01A2/GM/NIGMS NIH HHS; T32 GM008450/GM/NIGMS NIH HHS; T32GM008450-18/GM/NIGMS NIH HHS; U19 AI067798/AI/NIAID NIH HHS; U19-AI067798/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Cytokines
Comments/Corrections

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