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10.1097/SLA.0b013e3181bfda1c

http://scihub22266oqcxt.onion/10.1097/SLA.0b013e3181bfda1c
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20032720!ä!20032720

suck abstract from ncbi


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pmid20032720      Ann+Surg 2010 ; 251 (1): 120-6
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  • Stat 6-dependent induction of myeloid derived suppressor cells after physical injury regulates nitric oxide response to endotoxin #MMPMID20032720
  • Munera V; Popovic PJ; Bryk J; Pribis J; Caba D; Matta BM; Zenati M; Ochoa JB
  • Ann Surg 2010[Jan]; 251 (1): 120-6 PMID20032720show ga
  • OBJECTIVE: To delineate the role of T-helper 2 (Th2) cytokines in the induction of trauma induced myeloid suppressor cells (TIMSC) and the regulation of nitric oxide production. BACKGROUND: Trauma induces myeloid cells that express CD11b+/Gr1+ and arginase 1 and exhibit an immune suppressing activity. This article explores the mechanisms that induce TIMSC and the effects on nitric oxide production in response to endotoxin. METHODS: TIMSC were studied in response to Th2 cytokines and a subsequent challenge to endotoxin. The role of Th2 cytokines was studied in STAT6-/- mice. Accumulation of TIMSC in spleens was studied using flow cytometry and immunhistochemistry. Plasma was recovered to measure accumulation of nitric oxide metabolites. RESULTS: TIMSC accumulated in the spleen of injured mice and were particularly sensitive to IL-4 and IL-13 with large inductions of arginase activity. Significant blunting in both the accumulation of TIMSC in the spleen and induction of arginase 1 was observed in STAT6-/- mice after physical injury. Accumulation of nitric oxide metabolites to endotoxin was observed in STAT6-/- mice. CONCLUSION: This study shows that induction of CD11b+/Gr1+ cells after physical injury play an essential role in the regulation of nitric oxide production after a septic challenge. The accumulation and induction of arginase 1 in TIMSC is Th2 cytokine dependent. To our knowledge, the role of TIMSC in the regulation of nitric oxide is a novel finding. This observation adds to the possibility that TIMSC could play an important role in immunosuppression observed after physical injury.
  • |Animals[MESH]
  • |Arginase/metabolism[MESH]
  • |CD11b Antigen/metabolism[MESH]
  • |Cells, Cultured[MESH]
  • |Endotoxins/*pharmacology[MESH]
  • |Enzyme Induction[MESH]
  • |Flow Cytometry[MESH]
  • |Immune Tolerance[MESH]
  • |Immunohistochemistry[MESH]
  • |Interleukin-13/immunology/metabolism[MESH]
  • |Interleukin-4/immunology/metabolism[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Mice, Inbred BALB C[MESH]
  • |Mice, Knockout[MESH]
  • |Myeloid Cells/immunology/*metabolism[MESH]
  • |Nitric Oxide/*metabolism[MESH]
  • |Receptors, Chemokine/metabolism[MESH]
  • |STAT6 Transcription Factor/*pharmacology[MESH]
  • |Signal Transduction/drug effects[MESH]
  • |Spleen/cytology[MESH]
  • |Th2 Cells/immunology/metabolism[MESH]


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