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PubMed1991

rIL-1 alpha enhances adoptive transfer of resistance to Listeria monocytogenes infection.

We have previously demonstrated that administration of recombinant rIL-1 alpha enhances resistance against Listeria monocytogenes infection in mice. In this study we considered the possibility that this cytokine might also augment adoptive immunity conferred by the transfer of listeria-immune spleen cells. Concomitant administration of rIL-1 alpha with large numbers (2 x 10(7) or 10(8)) of listeria-immune spleen cells reduced the protection mediated by the transferred cells. Conversely, rIL-1 alpha co-administered with suboptimal numbers (1-5 x 10(6)) of immune splenocytes augmented anti-listeria resistance in an additive fashion. Although transfer of 10(6) listeria-immune spleen cells alone did not result in significant protection, when 10(6) immune cells were incubated with rIL-1 alpha prior to transfer they conferred significant protection to naive recipients. Time course experiments indicated that the greatest protection was achieved when listeria-immune spleen cells were pretreated with rIL-1 alpha for 2 h prior to adoptive transfer. The protection transferred by 10(6) rIL-1 alpha-pretreated immune spleen cells was not inhibited by TGF beta. This study is the first to use rIL-1 alpha to potentiate the adoptive transfer of resistance to an infectious agent by immune cells.

Animals↗
PubMed1994

Host cell responses to Listeria monocytogenes infection include differential transcription of host stress genes involved in signal transduction.

We examined the effect of Listeria monocytogenes infection of J774 macrophage-like mouse cells on induction of several stress genes, including genes for heat shock proteins (HSPs) and a protein-tyrosine phosphatase (PTP), to understand the host response in various steps of the bacterial invasion process. Exposure to wild-type L. monocytogenes strain EGD elicited an early induction of HSP70 mRNA with a corresponding early appearance of HSP70 protein. Cytochalasin D pretreatment prevented the induction of HSP70 mRNA in L. monocytogenes-infected macrophages. After a 2-hr infection with L. monocytogenes, PTP and to a lesser extent HSP90 mRNA levels were elevated. A listeriolysin-negative mutant of L. monocytogenes strain EGD and a noninvasive species of Listeria, Listeria innocua, did not induce PTP or HSP90 mRNA in infected macrophages. Mutations in other virulence genes did not affect transcription of PTP or HSP90. Expression of HSP60 mRNA remained constant over the time course studied in wild-type or mutant strains. These results suggest that phagocytosis of L. monocytogenes triggers transcription of HSP70 mRNA in macrophages; however, escape from the phagosome appears to be necessary for induction of PTP and HSP90 mRNA. Since both PTP and HSP90 may have links with signal transduction pathways in eukaryotic cells, the induction of these mRNAs suggests a role for L. monocytogenes in influencing the signal transduction routes of the host cell.

Animals↗
PubMed1992

Dissociation of macrophage cytolysis and ability to transfer anti-listeria resistance by concanavalin A-stimulated spleen cells.

In this study, we determined whether spleen cells from Listeria monocytogenes-immunized mice were cytolytic for Listeria-infected macrophages. Spleen cells freshly obtained from immunized donors were unable to lyse Listeria-infected macrophages unless they were first stimulated in vitro for 2-3 days with Concanavalin A (ConA) or L. monocytogenes. Spleen cells from non-immunized mice developed cytolytic activity after incubation with ConA, but not with L. monocytogenes. Cytolytic spleen cells demonstrated an equivalent ability to lyse uninfected and Listeria-infected thioglycollate elicited peritoneal macrophages. Maximal cytolysis required co-incubation of effector and target cells for 18-20 h. Spleen cell culture supernatants did not lyse macrophages, suggesting that cytolysis required direct contact. Preincubation of immune spleen cells with ConA decreased their ability to transfer anti-listeria resistance in the spleens, but not the livers of recipient mice. Depletion of CD4+ or CD8+ cells did not significantly reduce the ability of ConA-incubated Listeria-immune spleen cells to transfer resistance. Despite being cytolytic for Listeria-immune infected macrophages, ConA-stimulated non-immune spleen cells did not transfer anti-listeria resistance. These results indicate that cytolytic cells can be generated by short-term incubation of spleen cells with antigen or mitogen. The dissociation between in vitro cytolytic activity and ability to transfer protection, however, suggests that the two biological activities are not inextricably linked.

Animals↗
PubMed1992

Kinetic analysis of cytokine gene expression in the livers of naive and immune mice infected with Listeria monocytogenes. The immediate early phase in innate resistance and acquired immunity.

The anamnestic response to infection with Listeria monocytogenes is characterized by the rapid elimination of normally lethal doses of bacteria and accelerated granuloma formation. These phenomena are mediated by listeria-specific memory T cells within the first 24 h after reinfection. In order to elucidate the mechanisms operative during this decisive phase of infection, we conducted a comprehensive kinetic and quantitative analysis of cytokine gene expression in the livers of naive and immune mice. Organs were removed at 30 min, and 1, 2, 6, and 24 h after primary and secondary infections, and PCR3-assisted messenger RNA (mRNA) amplification was performed on matched samples using primers specific for IL-1 beta, IL-6, M-CSF, GM-CSF, TNF-alpha, IFN-gamma, IL-10, IL-4, IL-2, IL-3 and I1-2Rp55. The cytokine pattern characteristic of secondarily infected animals differed qualitatively by the expression of mRNA for IL-2, IL-2Rp55, IL-3, and IL-4, demonstrating the accumulation and activation of specific T cells in the livers as early as 1 to 2 h after reinfection. Combined in vivo depletion of both CD4+ and CD8+ T cells before reinfection almost completely abrogated the differentiated cytokine profile typical of the anamnestic response. Using competitive PCR for semiquantitative determination of mRNA levels, the amount of IL-1 beta and IL-6 mRNA was found to be very similar during primary and secondary infection, whereas TNF-alpha mRNA was found to be increased by approximately 10-fold 2 h and IFN-gamma mRNA by approximately 50 to 100-fold 6 h after reinfection when compared with a primary challenge. Combined in vivo depletion of both CD4+ and CD8+ T cells before reinfection resulted in a substantial (approximately 10-fold) decrease in IFN-gamma mRNA expression. To correlate these findings with cytokine secretion, spleen cells from naive and immune as well as normal and CD4+ and CD8+ cell depleted mice infected 6 h previously were cultured for 48 h, and supernatants were analyzed for the amount of the above mentioned cytokines. Semiquantitative PCR-assisted mRNA amplification is demonstrated to be a superior tool in dissociating the mediators of innate resistance from those operative in protective immunity and granuloma formation.

Animals↗
PubMed1993

The effect of adult thymectomy on immune response to infection with Listeria monocytogenes in mice.

The role of adult thymus in in vivo immune response to infection with Listeria monocytogenes was examined using euthymic mice and adult-thymectomized (ATx) mice which had been thymectomized 2 weeks before. Numbers of T cells in peritoneal cavities and spleens were increased at 2 weeks after inoculation of L. monocytogenes, whereas such increases of T cells were several times higher in euthymic mice than in ATx mice. In flow-cytometric analysis of peritoneal exudate cells, a significant increase of CD3+CD4-CD8- cells bearing gamma/delta type T cell receptor was noted in euthymic mouse after infection compared to ATx mouse. Neither assay of antigen-specific T cell proliferation nor analysis of cell cycle exhibited any superiority of T cells obtained from euthymic mice to those obtained from ATx mice. These findings suggest that the enlargement of T cell population in euthymic mice is attributed largely to T cells which emigrate from the thymus after inoculation of L. monocytogenes. Moreover, in vivo protective immune response against secondarily challenged L. monocytogenes was achieved more efficiently in euthymic mice than in ATx mice, as shown by the clearance of the bacteria from organs and the survival rate of infected mice. Our results indicate the importance of adult thymus-dependent increase of T cells in eliminating the facultative intracellular bacteria such as L. monocytogenes.

Animals↗
PubMed1996

Early pathogenesis of Listeria monocytogenes infection in the mouse spleen.

Histological observations suggested that in the spleen, blood-borne Listeria monocytogenes bacteria were preferentially ingested by two morphologically distinct mononuclear phagocyte populations present in the marginal zone of the white pulp. The morphologies of these phagocytes corresponded to those of marginal zone macrophages or marginal zone dendritic cells. Moreover, during the first day of infection, the same phagocytes containing listeria apparently translocated from the marginal zone into the white pulp where they established secondary infectious foci. This event was associated with a large influx of neutrophil polymorphonuclear leucocytes (PMNLs) into infected white pulp, and with the disappearance of lymphocytes from this compartment. White pulp lymphocytopenia also occurred in the spleens of listeria-infected mice selectively depleted of neutrophil PMNLs, indicating that these phagocytes were not responsible for displacing or destroying lymphocytes. The implications of these findings for explaining the virulence and immunogenicity of L. monocytogenes are discussed.

Animals↗
PubMed1994

[Host defense and endogenous interferon-gamma in the intestines during an oral infection with Listeria monocytogenes].

It is well known that IFN-gamma is crucial in the host defense against an intravenous infection with Listeria monocytogenes in mice. Recent studies have shown that listeriosis is caused by a food-born infection. Therefore, the production and role of IFN-gamma in the small intestines of intragastric infected-mice were investigated. On day 1 of infection, the number of bacteria cells in the feces peaked and endogenous IFN-gamma was detected in the small intestines by the immunohistochemical method, suggesting that host responses involving IFN-gamma production might occur in the early phase of infection in the small intestines. By FACS analysis, intraepithelial lymphocytes (IEL) were mainly CD3+CD8+ T cells and TCR-gamma delta+ cells were observed frequently in IEL. IFN-gamma producing cells could be detected in intestinal IEL of mice by ELISPOT assay. The analysis by reverse transcription-polymerase chain reaction analysis showed that IFN-gamma mRNA was detected in IEL of the infected mice, whereas the expression of IFN-gamma mRNA was suppressed in IEL of the mice treated with anti-CD8 mAb or anti-Thy1.2 mAb. These results suggested that Thy-1+CD+TCR-gamma delta+ T cells might be the principal source of IFN-gamma production in IEL of the infected mice. Administration of anti-IFN-gamma mAb resulted in suppression of anti-listerial resistance in the intestines. Furthermore, administration of anti-CD 8 mAb resulted in suppression of the local anti-listerial resistance on day 1 of infection. These results suggest that IFN-gamma is produced in IEL and might play a protective role in Listeria monocytogenes in the small intestines.

Animals↗
PubMed1997

Responses by murine macrophages infected with Listeria monocytogenes crucial for the development of immunity to this pathogen.

Macrophages and other mammalian cells respond to infection with Listeria monocytogenes (L. monocytogenes) by the transient or persistent activation of host cell signal transduction pathways. In addition, L. monocytogenes infection influences expression of various host cell genes, such as stress genes, genes from the MHC I and II complex, cytokine genes, and cytokine receptor genes. The possible influences of the different host cell responses on the outcome of an L. monocytogenes infection in vitro as well as for the development of immunity are discussed.

Animals↗
PubMed2006

Infection with Listeria monocytogenes as a probe for placental immunological function.

This chapter will describe the use of infection with Listeria monocytogenes, a Gram-positive intracellular bacterium, to study immunological responses in the placenta. This bacterium is chosen because it has a predilection for replication in the placenta. As such, it is a significant pathogen for pregnant women, being a major cause of fetal mortality and morbidity if appropriate public health precautions are not observed. Furthermore, this bacterium has been a major tool for studying innate immune responses and their transition to an acquired one, characterized by a Th1-type response. Details are given for the culture and maintenance of bacteria stocks, infection of mice, and analysis of the resultant infection. Such studies have revealed a unique pattern of immune responses in the placenta that, through the methods described, should reveal the strategies that the placenta uses to eradicate pathogens while not rejecting allogenic fetuses.

Animals↗
PubMed1998

Central nervous system infection with Listeria monocytogenes. 33 years' experience at a general hospital and review of 776 episodes from the literature.

We reviewed 776 previously reported and 44 new cases of CNS listeriosis outside of pregnancy and the neonatal period, and evaluated the epidemiologic, diagnostic, and therapeutic characteristics of this infection. Among patients with Listeria meningitis/meningoencephalitis, hematologic malignancy and kidney transplantation were the leading predisposing factors, but 36% of patients had no underlying diseases recognized. The infection occurred throughout life, with a higher incidence before the age of 3 and after the age of 45-50 years. Fever, altered sensorium, and headache were the most common symptoms, but 42% of patients had no meningeal signs on admission. Compared with patients with acute meningitis due to other bacterial pathogens, patients with Listeria infection had a significantly lower incidence of meningeal signs, and the CSF profile was significantly less likely to have a high WBC count or a high protein concentration. Gram stain of CSF was negative in two-thirds of cases of CNS listeriosis. One-third of patients had focal neurologic findings, and approximately one-fourth developed seizures over their course. Mortality was 26% overall, and was higher among patients with seizures and those older than 65 years of age. Relapse occurred in 7% of episodes. Ampicillin for a minimum of 15-21 days (with an aminoglycoside for at least the first 7-10 days) remains the treatment of choice. Cerebritis/abscess due to L. monocytogenes, without meningeal involvement, is less common but may be diagnosed by blood cultures and CNS imaging, or by stereotactic biopsy. Longer antibiotic therapy (at least 5-6 weeks) is needed in the presence of localized CNS involvement.

Brain Abscess↗
PubMed2002

Mechanism of murine Vgamma1+ gamma delta T cell-mediated innate immune response against Listeria monocytogenes infection.

Murine gamma delta T cells participate in innate immune response against infection of the intracellular bacterium Listeria monocytogenes. In the present report, we analyzed the mechanism of the gamma delta T cell-mediated response against L. monocytogenes infection. gamma delta T cell-enriched spleen cells of L. monocytogenes-infected mice produced IFN-gamma in vitro in response to L. monocytogenes-infected spleen cells. The IFN-gamma production was abrogated by depletion of Vgamma1+ gamma delta T cells. IFN-gamma production of the Vgamma1+ gamma delta T cells in response to L. monocytogenes-infected spleen cells required IL-12. However, addition of Fab fragment of anti-TCR gamma delta monoclonal antibodies (mAb) failed to block the response, suggesting that the response requires no TCR-mediated antigen recognition. Interestingly, Vgamma1+ gamma delta T cells of naive mice also produced IFN-gamma in response to L. monocytogenes-infected spleen cells in an IL-12-dependent manner. Furthermore, the IL-12 receptor (IL-12R) gene was expressed on the Vgamma1+ gamma delta T cells of naive mice as well as those of L. monocytogenes-infected mice although naive alpha beta T cells lack IL-12R expression. All the results suggest that the Vgamma1+ gamma delta T cells participate in immune surveillance against intracellular bacterial infection through quick production of IFN-gamma in response to infection-induced IL-12 without antigen-driven clonal expansion and maturation.

Animals↗
PubMed1985

Effect of aging on antimicrobial immunity: old mice display a normal capacity for generating protective T cells and immunologic memory in response to infection with Listeria monocytogenes.

Old (19 to 30 mo) and young adult (11 to 16 wk) AB6F1 mice of both sexes were compared in terms of their capacity to resist infection with Listeria monocytogenes. The LD50 was found to be two to four times higher for old than for young mice, and the time to death was longer for old mice. Enumeration of bacteria in the livers and spleens showed that old mice restricted growth of Listeria more effectively than young mice during the preimmune phase of infection, the difference being detectable as early as 12 to 24 hr after bacterial inoculation. Therefore, to ensure a similar level of infection in old and young mice, old mice had to be given a larger inoculum. Indeed, it was found that, provided the size of the bacterial inoculum was adjusted to make the level of immunizing infection the same, old mice generated similar levels of anti-Listeria immunity as young mice, as measured by their ability to generate splenic T cells capable of adoptively immunizing young recipients against lethal challenge infection. Furthermore, the level of memory immunity to reinfection 28 to 117 days after immunizing infection was similar in old and young mice. The results indicate, therefore, that old mice have no defect in their capacity to generate T cell-mediated anti-Listeria immunity.

Aging↗
PubMed2005

Autistic effector T cells in mice with a point mutation in the LAT adaptor fail to respond to Listeria monocytogenes infection.

The adaptor protein linker for activation of T cells (LAT) is an important transducer of extracellular T cell stimuli. In mice with a point mutation in LAT (LatY136F), TCR signaling is substantially compromised and LatY136F T cells are unresponsive to CD3 cross-linking in vitro. Nevertheless, LatY136F mice develop a polyclonal lymphoproliferation of CD4(+) T cells, which display a T(h)2-polarized effector phenotype. In this study, LatY136F mice were infected with the intracellular bacterium Listeria monocytogenes and the antigen-specific responses of T cells were determined. Both CD4(+) and CD8(+) LatY136F T cells were unresponsive to L. monocytogenes infection. In contrast, when CD4(+) T cells from wild-type mice were adoptively transferred into LatY136F hosts, they responded normally to L. monocytogenes, indicating that the LatY136F milieu permits T(h)1 responses. Furthermore, we analyzed whether the infection would influence the capacity of LatY136F CD4(+) T cells to produce IL-4 and IFN-gamma. While L. monocytogenes infection results in T(h)1-type T cell responses in wild-type animals, we found that it did not shift the strong T(h)2 polarization of LatY136F T cells towards a T(h)1 pattern. In conclusion, our results suggest that the activation and T(h)2 polarization of the LatY136F CD4(+) T cells is not influenced by infection with an intracellular pathogen known to induce robust T(h)1 responses, and is thus likely driven by T cell intrinsic mechanisms.

Adaptor Proteins, Signal Transducing↗
PubMed1974

Effects of Dextran Sulfate 500 on Cell-Mediated Resistance to Infection with Listeria monocytogenes in Mice.

Injection of dextran sulfate 500 caused loss of antibacterial resistance. Mice became more susceptible to an infection with Listeria monocytogenes and were unable to develop antilisterial immunity after both active and passive immunization with passively administered spleen cells from Listeria-immune donors. Indirect evidence suggests that the phagocytic component of cell-mediated resistance to bacterial infection is the site of attack of dextran sulfate.

Journal Article↗
PubMed1994

Administration of antigranulocyte monoclonal antibody RB6-8C5 prevents expression of acquired resistance to Listeria monocytogenes infection in previously immunized mice.

Recent studies have established the importance of neutrophils in innate resistance to Listeria monocytogenes infection in mice. The purpose of this study was to determine the importance of neutrophils in acquired resistance to L. monocytogenes infection. Previously immunized mice that were depleted of neutrophils by administration of the antigranulocyte monoclonal antibody RB6-8C5 demonstrated less resistance to L. monocytogenes challenge than did nonimmunized control mice. In contrast, immunized control mice exhibited a heightened resistance to rechallenge, as expected. These results suggest that neutrophils make previously unrecognized contributions to acquired immunity to a facultative intracellular pathogen.

Animals↗
PubMed1995

Unique order of the lymphocyte subset induction in the liver and intestine of mice during Listeria monocytogenes infection.

We investigated how NK cells, extrathymic T cells, and thymus-derived T cells are activated in mice during infection with an intracellular pathogen, Listeria (L.) monocytogenes. Although macrophages and granulocytes are known to be involved in the elimination of this pathogen in an early phase of infection, it was still controversial what type of lymphocytes are induced as effectors in subsequent phases. When mice were ip injected with 1 x 10(3) L. monocytogenes (a sublethal dose), a prominent increase in the number of mononuclear cells in the liver and spleen was induced. Phenotypic analysis revealed that serial induction of lymphocyte subsets, NK cells-->extrathymic T cells-->thymus-derived T cells, occurred in these organs. Extrathymic T cells were estimated to have intermediate CD3 and a high level of IL-2 receptor beta-chain on the surface (i.e., intermediate CD3 cells). These mice became free from infection after 2 weeks. In the case of oral administration, 1 x 10(3) L. monocytogenes increased the number of cells in the liver and the number of intraepithelial and lamina propria lymphocytes in the intestine. Phenotypic analysis also showed a sequential induction of lymphocyte subsets in the liver and the induction of extrathymic T cells in the intestine. Preelimination of intermediate TCR cells and NK cells by in vivo treatment with anti-LFA-1 mAb made mice susceptible to an ip injected sublethal dose of L. monocytogenes. These results reveal a unique order of lymphocyte induction during listerial infection and indicate that extrathymic T cells might be one of the important cells in achieving resistance against L. monocytogenes.

Animals↗
PubMed2005

Murine pulmonary infection with Listeria monocytogenes: differential susceptibility of BALB/c, C57BL/6 and DBA/2 mice.

Murine listeriosis is a paradigm to understand host pathogen interactions. Airway infections with Listeria monocytogenes, although representing a serious problem in early onset neonatal listeriosis, has not been investigated in detail in animal models so far. Here, the susceptibility of BALB/c, DBA/2 and C57BL/6 mice towards an intratracheal (i.t.) infection with virulent L. monocytogenes EGDe and the attenuated variant L. monocytogenes EGD hlyW491A(pERL3-CMVGFP) is reported. The course of infection was characterized by determination of bacterial numbers in the organs and assessment of the health condition of the mice. The distribution and cellular localization of Listeria in the airways was assessed by immunocytochemistry and confocal and electron microscopy. The differential susceptibility of inbred mouse strains to airway infections with L. monocytogenes could be assigned to the major virulence factor listeriolysin O. Resistant C57BL/6 mice were not affected by the two listerial strains. In contrast, BALB/c and DBA/2 mice showed differential susceptibility towards L. monocytogenes EGDe and attenuated bacteria, with all the mice being killed by the wild-type bacteria but rarely by the variant that secretes a listeriolysin of only 10% activity of that of the wild-type toxin. Thus, listeriolysin is a decisive factor for differential susceptibility against Listeria. After i.t. application, bacteria were predominantly localized in the peribronchiolar space and invaded alveolar macrophages but rarely lung epithelial cells. Dissemination from the lung into the deep organs started almost immediately after application, although a pulmonary bacterial reservoir remained during the first 4 days.

Animals↗