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

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 microgram/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 10(10) 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.