Granulocyte colony-stimulating factor: Release is not impaired after burn wound infection

被引:4
作者
Gamelli, R [1 ]
He, LK [1 ]
Hahn, E [1 ]
机构
[1] Loyola Univ, Med Ctr, Dept Surg, Burn & Shock Trauma Inst, Maywood, IL 60153 USA
来源
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE | 2002年 / 53卷 / 02期
关键词
granulocyte colony-stimulating factor (G-CSF); burn; infection; granulocytopoiesis;
D O I
10.1097/00005373-200208000-00016
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
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. Conclusion: 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.
引用
收藏
页码:284 / 289
页数:6
相关论文
共 33 条
[1]  
ALEXANDER J W, 1970, Surgery Gynecology and Obstetrics, V130, P431
[2]   CHARACTERIZATION OF A SERUM FACTOR STIMULATING THE DIFFERENTIATION OF MYELOMONOCYTIC LEUKEMIC-CELLS [J].
BURGESS, AW ;
METCALF, D .
INTERNATIONAL JOURNAL OF CANCER, 1980, 26 (05) :647-654
[3]  
CHATTA GS, 1994, BLOOD, V84, P2923
[4]   GRANULOCYTE-COLONY-STIMULATING FACTOR - ROLE AND RELATIONSHIPS IN INFECTIOUS-DISEASES [J].
DALE, DC ;
LILES, WC ;
SUMMER, WR ;
NELSON, S .
JOURNAL OF INFECTIOUS DISEASES, 1995, 172 (04) :1061-1075
[5]   THE KINETICS OF MURINE HEMATOPOIETIC STEM-CELLS IN-VIVO IN RESPONSE TO PROLONGED INCREASED MATURE BLOOD-CELL PRODUCTION INDUCED BY GRANULOCYTE-COLONY-STIMULATING FACTOR [J].
DEHAAN, G ;
DONTJE, B ;
ENGEL, C ;
LOEFFLER, M ;
NIJHOF, W .
BLOOD, 1995, 86 (08) :2986-2992
[6]   Granulocyte colony-stimulating factor receptors on granulocytes are down-regulated after endotoxin administration to healthy humans [J].
Dekkers, PEP ;
Juffermans, NP ;
ten Hove, T ;
de Jonge, E ;
van Deventer, SJH ;
van der Poll, T .
JOURNAL OF INFECTIOUS DISEASES, 2000, 181 (06) :2067-2070
[7]  
DEMETRI GD, 1991, BLOOD, V78, P2791
[8]   MACROPHAGE SUPPRESSION OF GRANULOCYTE AND MACROPHAGE GROWTH FOLLOWING BURN WOUND-INFECTION [J].
GAMELLI, RL ;
HE, LK ;
LIU, H .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1994, 37 (06) :888-892
[9]   Burn wound infection-induced myeloid suppression:: The role of prostaglaodin E2, elevated adenylate cyclase, and cyclic adenosine monophosphate [J].
Gamelli, RL ;
He, LK ;
Liu, H ;
Ricken, JD .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1998, 44 (03) :469-474
[10]   MARROW GRANULOCYTE-MACROPHAGE PROGENITOR-CELL RESPONSE TO BURN INJURY AS MODIFIED BY ENDOTOXIN AND INDOMETHACIN [J].
GAMELLI, RL ;
HE, LK ;
LIU, H .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1994, 37 (03) :339-346