Treatment with recombinant granulocyte colony‐stimulating factor (FilgrastinTM) stimulates neutrophils and tissue macrophages and induces an effective non‐specific response against Mycobacterium avium in mice

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Abstract
A role of neutrophils in the host response against Mycobacterium avium (MAC) has recently been suggested. To investigate this matter further, we determined the effect of granulocyte colony-stimulating factor (G-CSF) on the outcome of MAC infection in mice. C57BL/6 bg+/bg− black mice were intravenously infected with 1×107 MAC and then divided into four experimental groups to receive G-CSF as follows: (i) 10 μg/kg/day; (ii) 50 μg/kg/day; (iii) 100 μg/kg/day; (iv) placebo control. Mice were killed at 2 and 4 weeks of treatment to determine the bacterial load of liver and spleen. Treatment with G-CSF at both 10 and 50 μg/kg/day doses significantly decreased the number of viable bacteria in liver and spleen after 2 weeks (≈70·5% and 69·0%, respectively), and after 4 weeks (≈53% and 52%, respectively, Pex vivo. Neutrophils and macrophages from G-CSF-treated mice were able to inhibit the growth of or to kill MAC ex vivo, while phagocytic cells from untreated control mice had no anti-MAC effect. These results suggest that activation of neutrophils appears to induce an effective non-specific host defence against MAC, and further studies should aim for better understanding of the mechanisms of protection.

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