title: Granulocyte colony-stimulating factor: release is not impaired after burn wound infection.
abstract: BACKGROUND
  The production of granulocyte colony-stimulating factor (G-CSF), the lineage specific essential regulator of neutrophil progenitor cell proliferation and differentiation, has been thought to be impaired in the setting of burn infection. The ability to directly measure murine G-CSF allows the further delineation of the G-CSF response in a clinically relevant model of thermal injury and infection.
  
  
  METHODS
  We used a commercially available solid phase enzyme-linked immunoabsorbent assay to quantify G-CSF production after burn wound infection in mice. Bone marrow cells, splenic cells, and serum were obtained from BDF1 mice on day 3 after a 15% total body surface area full-thickness scald burn with or without Pseudomonas aeruginosa burn wound infection. G-CSF production of bone marrow cells or splenic cells and the serum level of G-CSF were measured. A clonogenic assay of bone marrow and spleen granulocyte-macrophage progenitor cells as well as blood leukocyte counts were also performed.
  
  
  RESULTS
  After burn sepsis, we noted that G-CSF production of the bone marrow and spleen was significantly increased; the numbers of progenitor cells in bone marrow and spleen were markedly enhanced; serum values of G-CSF were 14 times greater than control values; serum colony-stimulating activity was greater than in control mice; and total blood leukocyte counts were significantly depressed.
  
  
  CONCLUSIONS
  These findings support the notion that granulocytopoietic failure after burn sepsis is not significantly related to defective endogenous G-CSF synthesis. More likely, hyporesponsiveness of granulocyte progenitor cells to G-CSF, changes in the relative balance of granulocyte versus monocyte progenitors within the granulocyte-macrophage progenitor cell compartment, and enhanced release of monocyte lineage specific growth factors are the critical elements responsible for burn infection-induced hematopoietic failure.
authors.affiliation: Department of Surgery, Loyola University Medical Center, Burn & Shock-Trauma Institute, Maywood, Illinois 60153, USA. rgamell@wpo.it.luc.edu
authors.forename: Richard
authors.initials: R
authors.lastname: Gamelli
authors.forename: Li-Ke
authors.initials: LK
authors.lastname: He
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Hahn
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001853:Bone Marrow / Q000378:metabolism; D002056:Burns / Q000150:complications / Q000276:immunology*; D002478:Cells, Cultured; D016179:Granulocyte Colony-Stimulating Factor / Q000096:biosynthesis* / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D011552:Pseudomonas Infections; D011897:Random Allocation; D018805:Sepsis / Q000209:etiology / Q000276:immunology*; D013154:Spleen / Q000378:metabolism
chemical_list: D016179:Granulocyte Colony-Stimulating Factor