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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]

Delayed footpad reactions and acquired cellular resistance to Listeria monocytogenes were studied in mice whose mononuclear phagocyte system (MPS) had been blocked or stimulated. Colloidal carbon was used for the blockade of MPS and Corynebacterium parrum used for the stimulation. Strong delayed footpad reactions. On the other hand, the i.v. rejection of 3 × 101; listeria induced an appreciable level mice, while in MPS-stimulated mice, i.v. injection with even 4 × 103; listeria could not induce such strong delayed footpad reaction. On the other hand, the i.v. injection of 3 × 10¹ listeria induced an appreciable level of delayed footpad reaction only in MPS-blocked mice. Acquired cellular resistance was depressed by MPS stimulation, whereas it was augmented by MPS blockade. These results suggested that non-specific activity of MPS modulates subsequent immune responses after inoculation of listeria. [ABSTRACT FROM AUTHOR]

We examined the host defence mechanism against infection with Listeria monocytogenes, a facultative intracellular bacterium, in mice with murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukaemia virus (MuLv) infection. Although LP-BM5 MuLV infection in C57BL/6 mice leads to a stage of immunodeficiency characterized by severe compromise of cell-mediated immunity, the mice with established MAIDS infected with LP-BM5 8 weeks previously, showed resistance to an intraperttoneal infection with Listeria monocytogenes. These MAIDS mice also showed resistance to a lethal dose of secondary listerial challenge, while the delayed-type hypersensitivity response to heat-killed Listeria (HKL) was severely impaired in MAIDS mice. The resistance of MAIDS mice to listerial infection was mediated by CD4+ αβ T cells but neither by γδ T cells nor natural killer (NK) cells. Interferon-γ (IFN-γ) and interleukin-10 (IL-10) were produced by CD4+ T ceils from Listeria-infected MAIDS mice in response tO the in vitro stimulation with HKL, whereas IFN-γ but not IL-10 were produced by those from Listeria-infected control mice. These results suggest that T-helper 0 (Th0)-like immune responses of CD4+ T cells occur and participate in host defence mechanisms against listerial infection in MAIDS mice. [ABSTRACT FROM AUTHOR]

We have previously reported that heat-shock protein (hsp) 60-reactive T-cell receptor (TCR)γδ+ T cells appear in the peritoneal cavity during the early stage of infection with Listeria monocytogenes in mice. In this study, we examined the kinetics of TCRγδ+ T cells during listeriosis in F344 ruts by flow cytometry using a V65 monoclonal antibody (mAb) directed to a constant determinant of rat TCRγδ chains. TCRγδ+ T cells significantly increased in the peritoneal cavity on day 6 and then decreased by day 10 after infection, in parallel with the kinetics of hsp 60 expression in the peritoneal macrophages during listeriosis in F344 rats. Most of the early appearing TCRγδ+ T cells were of the CD4- CD8αβ+ CD5+ lymphocyte function-associated antigen (LFA)-1αhigh CD45RC- interleukin-2 receptor (IL-2R) α- phenotype, although a significant fraction of the TCRγδ+ T cells expressed CD8σ only. The increase in TCRγδ+ T cells during listeriosis was prominent in F1 (F344 × Lewis) rats but only marginal in Lewis rats, which was correlated with the expression level of hsp 60 in the peritoneal macrophages. The peritoneal TCRγδ+ T cells in naive F344 rats appeared to proliferate significantly in response to recombinant hsp 60 (rhsp 60) derived from Mycobacterium bovis bacillus Calmette-Guérin (BCG). These results imply that the early appearance of hsp 60-reactive TCRγδ+ T cells during listerial infection can be generalized across species. [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]

Neonatally thymectomized (NTx) mice, whose ability to mount antigen-specific cell-mediated immunity is reported to be generally defective, were found to be capable of mounting a normal level of acquired cellular resistance (ACR) and delayed footpad reaction (DFR) to Listeria monocytogenes. The present study was done in order to determine the functional differences of T cells contributing to the protection against L. monocytogenes between NTx and sham-operated mice. In mice immunized with viable L. monocytogenes, the absolute number of splenic T cells was significantly lower in NTx mice compared with sham-operated mice. When the ability of immune T cells to transfer ACR and DFR was examined by passive transfer, lymphocytes from immune NTx mice conferred a higher level of ACR and DFR on naive recipient mice, despite the marked difference in total number of T cells compared with immune Sham mice. Antigen-specific proliferation and interleukin-2 (IL-2) production by splenic T cells from immune NTx mice were significantly lower than in those from immune Sham mice. The proliferative response of T cells to exogenous IL-2 was also lower in NTx group. These results suggest that the requirement for the IL-2-driven T-cell proliferation system is basically low in the generation of effector T cells specific for L. monocytogenes. [ABSTRACT FROM AUTHOR]