Granulocyte colony-stimulating factor enhances killing of translocated bacteria but does not affect barrier function in a burn mouse model

Tonyia Eaves-Pyles, J. Wesley Alexander

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Background: Granulocyte colony-stimulating factor drives the proliferation and differentiation of granulocytes and also enhances their bactericidal and phagocytic activity. The present study was undertaken to investigate the effects of murine granulocyte colony-stimulating factor (mG- CSF) on bacterial translocation and gut-derived sepsis after burn injury. Methods: In experiment I, BALB/c mice were randomized into two treatment groups, which received 1 μg/mouse of mG-CSF subcutaneously for either 1 (n = 16) or 2 days (n = 15). Controls received saline (n = 16). After treatment, all animals were gavaged with 1010 111In Escherichia coli and then given a 20% burn. All groups were observed 10 days for survival. In experiment II, three additional groups (n = 6/group) received the same treatment as above but were killed 4 hours after burn injury. Mesenteric lymph nodes, liver, and spleen were harvested to measure radionuclide counts (disintegrations per minute per gram of tissue) and colony-forming units (CFU/g of tissue) and to calculate the percentage of viable bacteria (% alive). Results: Experiment I: 10-day survival was significantly higher in groups treated with mG-CSF for 1 or 2 days (75% and 73%, respectively), compared with controls (43.7%), p = 0.001. Experiment II: no differences in translocation to the tissues were observed among any of the groups, according to radionuclide counts. However, quantitative colony counts and calculated percentage of viable bacteria showed that killing was enhanced in the mesenteric lymph nodes and liver of animals that received mG-CSF, but this was significant only in the liver for both treatment times (1 day, p = 0.021 and 2 day, p = 0.009). Conclusion: These data suggest that treatment with mG-CSF does not improve gut barrier function, but does enhance the host's ability to kill translocated organisms and improve survival in a gut-derived sepsis model.

Original languageEnglish (US)
Pages (from-to)1013-1017
Number of pages5
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume41
Issue number6
DOIs
StatePublished - Dec 1996
Externally publishedYes

Fingerprint

Granulocyte Colony-Stimulating Factor
Bacteria
Radioisotopes
Liver
Sepsis
Lymph Nodes
Bacterial Translocation
Macrophage Colony-Stimulating Factor
Wounds and Injuries
Granulocyte-Macrophage Colony-Stimulating Factor
Granulocytes
Stem Cells
Spleen
Escherichia coli

Keywords

  • Burn injury
  • Granulocyte colony-stimulating factor
  • Gut-derived sepsis
  • Translocation

ASJC Scopus subject areas

  • Surgery

Cite this

@article{37c969fb420d4d50a84ca68bb2537cd5,
title = "Granulocyte colony-stimulating factor enhances killing of translocated bacteria but does not affect barrier function in a burn mouse model",
abstract = "Background: Granulocyte colony-stimulating factor drives the proliferation and differentiation of granulocytes and also enhances their bactericidal and phagocytic activity. The present study was undertaken to investigate the effects of murine granulocyte colony-stimulating factor (mG- CSF) on bacterial translocation and gut-derived sepsis after burn injury. Methods: In experiment I, BALB/c mice were randomized into two treatment groups, which received 1 μg/mouse of mG-CSF subcutaneously for either 1 (n = 16) or 2 days (n = 15). Controls received saline (n = 16). After treatment, all animals were gavaged with 1010 111In Escherichia coli and then given a 20{\%} burn. All groups were observed 10 days for survival. In experiment II, three additional groups (n = 6/group) received the same treatment as above but were killed 4 hours after burn injury. Mesenteric lymph nodes, liver, and spleen were harvested to measure radionuclide counts (disintegrations per minute per gram of tissue) and colony-forming units (CFU/g of tissue) and to calculate the percentage of viable bacteria ({\%} alive). Results: Experiment I: 10-day survival was significantly higher in groups treated with mG-CSF for 1 or 2 days (75{\%} and 73{\%}, respectively), compared with controls (43.7{\%}), p = 0.001. Experiment II: no differences in translocation to the tissues were observed among any of the groups, according to radionuclide counts. However, quantitative colony counts and calculated percentage of viable bacteria showed that killing was enhanced in the mesenteric lymph nodes and liver of animals that received mG-CSF, but this was significant only in the liver for both treatment times (1 day, p = 0.021 and 2 day, p = 0.009). Conclusion: These data suggest that treatment with mG-CSF does not improve gut barrier function, but does enhance the host's ability to kill translocated organisms and improve survival in a gut-derived sepsis model.",
keywords = "Burn injury, Granulocyte colony-stimulating factor, Gut-derived sepsis, Translocation",
author = "Tonyia Eaves-Pyles and Alexander, {J. Wesley}",
year = "1996",
month = "12",
doi = "10.1097/00005373-199612000-00012",
language = "English (US)",
volume = "41",
pages = "1013--1017",
journal = "Journal of Trauma and Acute Care Surgery",
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T1 - Granulocyte colony-stimulating factor enhances killing of translocated bacteria but does not affect barrier function in a burn mouse model

AU - Eaves-Pyles, Tonyia

AU - Alexander, J. Wesley

PY - 1996/12

Y1 - 1996/12

N2 - Background: Granulocyte colony-stimulating factor drives the proliferation and differentiation of granulocytes and also enhances their bactericidal and phagocytic activity. The present study was undertaken to investigate the effects of murine granulocyte colony-stimulating factor (mG- CSF) on bacterial translocation and gut-derived sepsis after burn injury. Methods: In experiment I, BALB/c mice were randomized into two treatment groups, which received 1 μg/mouse of mG-CSF subcutaneously for either 1 (n = 16) or 2 days (n = 15). Controls received saline (n = 16). After treatment, all animals were gavaged with 1010 111In Escherichia coli and then given a 20% burn. All groups were observed 10 days for survival. In experiment II, three additional groups (n = 6/group) received the same treatment as above but were killed 4 hours after burn injury. Mesenteric lymph nodes, liver, and spleen were harvested to measure radionuclide counts (disintegrations per minute per gram of tissue) and colony-forming units (CFU/g of tissue) and to calculate the percentage of viable bacteria (% alive). Results: Experiment I: 10-day survival was significantly higher in groups treated with mG-CSF for 1 or 2 days (75% and 73%, respectively), compared with controls (43.7%), p = 0.001. Experiment II: no differences in translocation to the tissues were observed among any of the groups, according to radionuclide counts. However, quantitative colony counts and calculated percentage of viable bacteria showed that killing was enhanced in the mesenteric lymph nodes and liver of animals that received mG-CSF, but this was significant only in the liver for both treatment times (1 day, p = 0.021 and 2 day, p = 0.009). Conclusion: These data suggest that treatment with mG-CSF does not improve gut barrier function, but does enhance the host's ability to kill translocated organisms and improve survival in a gut-derived sepsis model.

AB - Background: Granulocyte colony-stimulating factor drives the proliferation and differentiation of granulocytes and also enhances their bactericidal and phagocytic activity. The present study was undertaken to investigate the effects of murine granulocyte colony-stimulating factor (mG- CSF) on bacterial translocation and gut-derived sepsis after burn injury. Methods: In experiment I, BALB/c mice were randomized into two treatment groups, which received 1 μg/mouse of mG-CSF subcutaneously for either 1 (n = 16) or 2 days (n = 15). Controls received saline (n = 16). After treatment, all animals were gavaged with 1010 111In Escherichia coli and then given a 20% burn. All groups were observed 10 days for survival. In experiment II, three additional groups (n = 6/group) received the same treatment as above but were killed 4 hours after burn injury. Mesenteric lymph nodes, liver, and spleen were harvested to measure radionuclide counts (disintegrations per minute per gram of tissue) and colony-forming units (CFU/g of tissue) and to calculate the percentage of viable bacteria (% alive). Results: Experiment I: 10-day survival was significantly higher in groups treated with mG-CSF for 1 or 2 days (75% and 73%, respectively), compared with controls (43.7%), p = 0.001. Experiment II: no differences in translocation to the tissues were observed among any of the groups, according to radionuclide counts. However, quantitative colony counts and calculated percentage of viable bacteria showed that killing was enhanced in the mesenteric lymph nodes and liver of animals that received mG-CSF, but this was significant only in the liver for both treatment times (1 day, p = 0.021 and 2 day, p = 0.009). Conclusion: These data suggest that treatment with mG-CSF does not improve gut barrier function, but does enhance the host's ability to kill translocated organisms and improve survival in a gut-derived sepsis model.

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