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Recombinant human granulocyte colony-stimulating factor (rh G-CSF) enhanced resistance of mice against Listeria monocytogenes (LM) as determined by survival and bacterial growth. Mice pretreated with rh G-CSF twice daily for 5 days survived better than untreated animals to the challenge with LM. Number of bacteria in peritoneal cavity (PC) and spleen was lower in treated mice than that in the control group. RhG-CSF increased mainly polymorphonuclear cells (PMN) in blood and spleen. After LM inoculation, a larger number of PMN and monocyte-macrophages accumulated in PC and spleen of tested mice. In addition, PMN primed in vivo with rh G-CSF released more superoxide anions when stimulated with phorbol myristate acetate. The inhibition of bacterial growth in PC and spleen could be ascribed to the accumulation of phagocytic cells at the infection sites and the increased oxidative metabolism. The results provided further evidence of the important contribution of G-CSF and neutrophils, as target cells, to the host defence against the intracellular bacteria. [ABSTRACT FROM AUTHOR]

We investigated the host defense mechanism in primary infection with Listeria monocytogenes in non-obese diabetic (NOD) mice at pre-diabetic stage showing an impaired responsiveness of the αβ T cells to T-cell receptor (TCR) triggering. The NOD mice showed a deteriorated resistance at the late stage after an intraperitoneal infection with L. monocytogenes compared with BALB/c and C57BL/6 mice as assessed by bacterial growth in organs. Consistent with our previous findings, a prominent increase in number of γδ T cells was evident at the early stage after infection, while generation of Listeria-specific αβ T cells was impaired in these mice. In vivo administration of anti-TCR γδ monoclonal antibody (mAb) allowed L. monocytogenes to grow exaggeratedly in the NOD mice. These results imply that γδ T cells may be mainly involved in protection against primary infection with L. monocytogenes in NOD mice. [ABSTRACT FROM AUTHOR]