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Results for “LISTERIA INFECTIONS”

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PubMed1994

Protection by dexamethasone from a lethal infection with Listeria monocytogenes in mice.

The effects of dexamethasone (DEX) on a lethal infection with Listeria monocytogenes were studied in mice. Mice were completely protected against the lethal infection when treated with 3.3 mg per kg of DEX. The effect was observed only when DEX was injected before infection. The control mice died from day 3 to day 5 of infection, whereas DEX-treated mice could eliminate L. monocytogenes cells from the organs by day 11 of infection. High titres of endogenous tumour necrosis factor (TNF), interleukin-6 (IL-6) and gamma interferon (IFN-gamma) were induced in the bloodstreams and organs of the drug-free mice. DEX suppressed IL-6 production, but augmented TNF and IFN-gamma production within 24 h of infection, whereas production of all three endogenous cytokines was suppressed in the DEX-treated mice on day 3 of infection when the control mice began to die. These results suggest that DEX shows a protective effect on a lethal infection with L. monocytogenes in mice and that regulation of production of endogenous cytokines might be involved in the effect of DEX.

Animals↗

PubMed1986

Toxicity and induction of resistance to Listeria monocytogenes infection by amphotericin B in inbred strains of mice.

Amphotericin B (AmB) treatment before infection with the bacterium Listeria monocytogenes prolonged survival of AKR mice but shortened survival of C57BL/6 mice compared with survival of untreated infected controls. C57BL/6 mice were also more sensitive to the acute toxic effects of AmB than AKR mice, as were (C57BL/6 X AKR)F1 hybrid mice. Spleen cells and erythrocytes (RBCs) from the C57BL/6 and the F1 hybrid mice were both more sensitive to the lytic and lethal effects of AmB than corresponding cells from AKR mice. Biochemical analysis indicated that catalase levels in RBCs from C57BL/6 and F1 hybrid mice were about 60% of those found in RBCs from AKR mice. The lysis by AmB of RBCs from all these strains of mice was inhibited by catalase or incubation in a low-oxygen environment. These findings suggest that (i) the low catalase levels in C57BL/6 and F1 hybrid mice may limit the protection of cells from the oxidant damage involved in AmB action, and (ii) the toxicity which occurs at low concentrations of AmB in the mouse strains with low intracellular catalase levels may interfere with or ablate the AmB-induced increases in mouse resistance to L. monocytogenes infection.

Amphotericin B↗

PubMed1999

T lymphocyte dynamics during Listeria monocytogenes infection.

Infection of mice with Listeria monocytogenes results in a robust T lymphocyte response that clears the pathogen and provides long term immunity from reinfection. The number of splenic CD4+ and CD8+ T cells and natural killer cells increases during primary and recall infection with L. monocytogenes, however the proportional increase is greatest for CD8+ T cells. The proportion of CD8 T cells expressing low levels of CD62L, a sign of activation, was increased among immune splenocytes, suggesting a substantial expansion of L. monocytogenes specific CTL. Analysis of CTL specific for the immunodominant LLO 91-99 epitope showed that essentially all were CD62Llo during the primary response, but that many upregulated expression of CD62L during the memory phase. Interestingly, the antigen specificity of nearly all additional CD62Llo CTL detected in spleens during recall L. monocytogenes infection can be accounted for with MHC class I tetramers complexed with four different epitopes. These studies demonstrate the complex T lymphocyte dynamics during infection with intracellular pathogens.

Animals↗

PubMed1986

Immunomodulatory effect of Listeria monocytogenes infection. II. Natural cell cytotoxicity in infected mice.

The natural cell cytotoxicity of blood leukocytes, splenocytes and peritoneal cells derived from Balb/c mice being on day 1, 3, 5, 7, 9 of listeriosis to allogeneic fibroblast L 929 was examined. The intensity of cytotoxic reaction was assessed by the per cent of specific 51Cr release from target cells. To check if this reaction correlates with the level of monocyte-macrophage lineage cells present in the effector cells of if it depends on the development of delayed type hypersensitivity to Listeria antigen, Balb/c mice were infected with Listeria monocytogenes and simultaneously treated with ATS. It was found that Listeria monocytogenes infection in mice enhanced the natural cell cytotoxicity of tested effectors cells, particularly of peritoneal cells in animals being on the 5th-7th day of listeriosis. The treatment of mice with ATS which is known to inhibit the development of delayed type hypersensitivity to Listeria antigen, completely suppressed the stimulatory effect of this infection on the natural cell cytotoxicity to allogeneic fibroblasts. This finding suggests that the enhancement of natural cytotoxic activity of tested effector cells results from the action of activated macrophages cooperating with Listeria sensitized T lymphocytes.

Animals↗

PubMed1989

[Involvement of the basal ganglia and brain stem in infection by Listeria monocytogenes. Anatomo-clinical study].

A case of a patient with haematogeneous infection by listeria monocytogenes, involving the basal and brainstem is reported. Clinically the disease manifested by fever and brainstem syndrome of acute onset. The microscopic examination revealed foci of suppurative encephalitis in the brainstem and basal ganglia. The possible pathogenic mechanisms are discussed. It is emphasized that the association of a febrile syndrome with brainstem dysfunction should raise the possibility of infection of the nervous system by listeria monocytogenes.

Adult↗

PubMed1980

Resistance to listeriosis in mice that are deficient in the fifth component of complement.

Infection with Listeria monocytogenes was studied in strains of mice with genetic absence of the fifth component of complement (C5). Mice deficient in C5 consistently showed an increased growth of Listeria in their spleens as compared to normal mice. This increased growth was not corrected by administration of plasma containing C5. Furthermore, depletion of C5 and terminal complement components by administration of cobra venom factor did not impair the resistance to Listeria infection of normal mice. No phagocytic defect could be detected in macrophages from strains lacking C5. Transfer of bone marrow cells from C5+ but not from C5- mice corrected the marked increase of Listeria growth in mice having blockade of the reticuloendothelial system. We hypothesize that the defect of mice lacking C5 lies not in the absence of serum C5 but somewhere at the level of the macrophage.

Animals↗

PubMed2006

[Neonatal infection with Listeria monocytogenes: rare, but serious].

Between 1993 and 2003, three infants, two girls and a boy, were found to have an invasive infection with Listeria monocytogenes. They received intensive care including respiratory and circulatory support, antibiotics, and treatment of the neurological complications when possible. One of the girls survived without sequelae but the other two infants died in the neonatal period. In one of these two cases there was a clear clue to the source of the infection in the dietary history of the mother: she had consumed unpasteurised cow's milk. The mothers ofthe infants that died had developed fever shortly before parturition. In The Netherlands, the incidence of neonatal invasive infection with Listeria is estimated at 1.3 per 100,000 live-born children per year. This figure seems not to have changed in the last 20 years. Because of the risk of this rare but serious infection, dietary advice to pregnant women to avoid possibly contaminated food is still relevant.

Animals↗

PubMed2005

Independent protective effects for tumor necrosis factor and lymphotoxin alpha in the host response to Listeria monocytogenes infection.

Although the essential role of tumor necrosis factor (TNF) in resistance to Listeria monocytogenes infection is well established, the roles of the related cytokines lymphotoxin alpha (LTalpha) and lymphotoxin beta (LTbeta) are unknown. Using C57BL/6 mice in which the genes for these cytokines were disrupted, we examined the contributions of TNF, LTalpha, and LTbeta in the host response to Listeria. To overcome the lack of peripheral lymph nodes in LTalpha(-/-) and LTbeta(-/-) mice, bone marrow chimeras were constructed. TNF(-/-) and LTalpha(-/-) chimeras that lacked both secreted LTalpha(3) and membrane-bound LTalpha(1)beta(2) and LTalpha(2)beta(1) were highly susceptible and succumbed 4.5 and 6 days, respectively, after a low-dose infection (200 CFU). LTbeta(-/-) chimeras, which lacked only membrane-bound LT, controlled the infection in a manner comparable to wild-type (WT) chimeras. The Listeria-specific proliferative and gamma interferon T-cell responses were equivalent in all five groups of infected mice (LTalpha(-/-) and LTbeta(-/-) chimeras, WT chimeras, and TNF(-/-) and WT mice). TNF(-/-) mice and LTalpha(-/-) chimeras, however, failed to generate the discrete foci of lymphocytes and macrophages that are essential for bacterial elimination. Rather, aberrant necrotic lesions comprised predominantly of neutrophils with relatively few lymphocytes and macrophages were observed in the livers and spleens of TNF(-/-) and LTalpha(-/-) chimeras. Therefore, in addition to TNF, soluble LTalpha(3) plays a separate essential role in control of listerial infection through control of leukocyte accumulation and organization in infected organs.

Animals↗

PubMed1998

Bone marrow cellular composition in Listeria monocytogenes infected mice detected using ER-MP12 and ER-MP20 antibodies: a flow cytometric alternative to differential counting.

Detailed assessment of bone marrow cellular composition is essential in the evaluation of various experimental in vivo systems, such as expression of transgenes, null mutations and stimulation of host defence in infection. Traditional morphological analysis of mouse bone marrow is laborious, requires specific cytological expertise, and is somewhat subjective. As an alternative, we have examined whether double labelling of bone marrow with the anti-precursor monoclonal antibodies ER-MP12 and ER-MP20 could be used for differential analysis by flow cytometry, as these antibodies define six relatively homogeneous cell populations in mouse bone marrow. Following a sublethal infection of mice with Listeria monocytogenes, we monitored changes in cellular composition of the bone marrow at various time points in three ways: differential morphological count; single-color flow cytometric analysis using markers for the myeloid, erythroid and lymphoid lineages; and double labelling with ER-MP12 and ER-MP20. As expected, the bone marrow composition changed dramatically during infection, leading to an increase of myeloid cells which peaked after 1 week of infection. Data determined by ER-MP12/20 flow cytometric analysis appeared to be in close agreement with both morphology and lineage marker analysis. In addition, ER-MP12/20 analysis provided more detailed information with regards to the presence of early myeloid precursors compared to lineage marker analysis. These data show that flow cytometric analysis of bone marrow using ER-MP12 and ER-MP20 monoclonal antibodies provides a relatively simple, rapid and objective assay when evaluating cellular composition in the bone marrow of the mouse.

Animals↗

PubMed1991

[Enhancement of host defence against infection with Listeria monocytogenes in newborn mice by various recombinant cytokines].

Neonatal mice within 24 h of birth were highly susceptible to infection of Listeria monocytogenes. The 50% lethal dose of bacterial cells for neonates and adult mice was 6.3 X 10(1) CFU and 3.2 x 10(6) CFU, respectively. A single intraperitoneal injection of recombinant murine interferon-gamma (rMuIFN-gamma) protected neonates from the simultaneous challenge with a lethal dose of L. monocytogenes. The protection of rMuIFN-gamma was consistently observed in neonates at doses more than 4 X 10(2) IU (0.1 micrograms protein) per mouse. The bacterial growth in the spleens and livers of neonates treated with rMuIFN-gamma was significantly suppressed in comparison with that in the untreated neonates. Furthermore, survived neonates from the infection with L. monocytogenes showed an acquired resistance against the intravenous injection of lethal dose of L. monocytogenes 4 weeks after the primary infection, and this resistance significantly increased in mice that had been treated with rMuIFN-gamma. In addition to rMuIFN-gamma, recombinant human interleukin-1 beta and recombinant human tumor necrosis factor -alpha were also effective on rescue from the lethal infection with Listeria monocytogenes in neonatal mice, but the effect was seen only in the limited doses. On the other hand, recombinant murine IFN-beta and recombinant human IL-2 were not effective at all. These results suggest that rMuIFN-gamma rather than other cytokines might endow neonatal mice with the enhanced antilisterial resistance involving macrophages and T lymphocytes.

Age Factors↗

PubMed1997

Both innate and acquired immunity to Listeria monocytogenes infection are increased in IL-10-deficient mice.

IL-10-deficient mice were highly resistant to Listeria monocytogenes during the course of infection. An increased innate immunity was suggested by reduced bacterial burdens (as much as 50-fold) early (days 2 and 3) in the infection, as compared with control mice. In addition, in vitro stimulation of both IL-10-deficient peritoneal exudate cells and spleen cells with heat-killed Listeria resulted in a dramatically enhanced proinflammatory cytokine response (e.g., IL-12, IFN-gamma, TNF-alpha, IL-1alpha, and IL-6). During later stages of a primary Listeria infection, the reduced bacterial burden in the infected organs of IL-10-deficient mice was accompanied by decreased tissue damage and earlier clearance of the pathogen, as well as a stronger Th1 polarization. The absence of IL-10 did not influence membrane-bound factors that stimulate Th cell responses, demonstrated by the finding of normal MHC class II, B7.1, and B7.2 surface expression on F4/80+ macrophages in vivo. IL-10-deficient mice were also more resistant to a secondary infection, accompanied by an enhanced Th1 response. The results presented in this work demonstrate that the absence of IL-10 augments innate and acquired immunity during primary and secondary L. monocytogenes infection by up-regulating proinflammatory type 1 cytokine responses. The resulting protective Th1 responses lead to an effective reduction of bacterial growth and tissue destruction and to an earlier clearance of the bacteria. The physiologic role of IL-10 during L. monocytogenes infection studies is discussed and compared with pathogenic infections that induce a more systemic cytokine response in IL-10-deficient mice.

Animals↗

PubMed1983

Fatal infection in mice after injection of immunosuppressive serum fractions from surgical patients.

Following surgical or accidental trauma many patients show suppression of cellular immunity. In this investigation sera from severely burned patients and patients undergoing aortic aneurysm repair were studied. Sera shown to suppress phytohaemagglutinin-induced blastogenesis of normal human lymphocytes were fractionated using ion exchange and G25 Sephadex chromatography. Suppressive activity was largely confined to a low molecular weight (LMW) fraction and was dose dependent. LMW fractions of normal sera had no significant suppressive activity. The purpose of this study was to test the causal relationship between immunosuppressive serum and decreased resistance to bacterial infection. Listeria monocytogenes infected mice were used as an in vivo model to test suppression of cellular immunity. Injection of LMW fractions of suppressive sera significantly increased mortality in these mice, but had no effect on non-infected mice. There was good correlation between the in vitro and in vivo effects of the suppressive fractions. These results suggest that a circulating factor in the serum of injured patients suppresses cellular immunity and may be responsible for impaired resistance to infection.

Adult↗

PubMedDate not supplied

[Inflammation and antibacterial resistance. III. Influence of an inflammatory reaction induced by the injection of polyacrylamide gels on the resistance of mice to Listeria monocytogenes infection].

Inflammation was induced in the dorsal area of pathogen-free mice following subcutaneous injection of polyacrylamide microbeads (Biogel) of varying particle size (200-400 mesh) and pore size (exclusion limit ranging from a molecular weight of 2,000 to 300,000). Six days after injection of the microbeads, mice were infected with 10(5) Listeria monocytogenes. Only animals injected with "Biogel P2, P4, P6" (exclusion limit 2,000, 4,000 and 6,000 respectively) survived this lethal inoculum of Listeria. A study of the kinetics of this increased resistance revealed that homogenates of granulomas, induced eight days before injection into mice, significantly decreased the number of listeria in the spleen of treated mice. Such increased resistance was not found in cell homogenates, but only in the exudate of 8-day old granulomas. Fractionation studies of the inflammatory exudates with ammonium sulfate showed that immunostimulating substance were present in the supernatant following precipitation with 80% saturated (NH4)2SO4.

Acrylic Resins↗

PubMed2004

Duration of infection and antigen display have minimal influence on the kinetics of the CD4+ T cell response to Listeria monocytogenes infection.

The T cell response to infection consists of clonal expansion of effector cells, followed by contraction to memory levels. It was previously thought that the duration of infection determines the magnitude and kinetics of the T cell response. However, recent analysis revealed that transition between the expansion and contraction phases of the Ag-specific CD8+ T cell response is not affected by experimental manipulation in the duration of infection or Ag display. We studied whether the duration of infection and Ag display influenced the kinetics of the Ag-specific CD4+ T cell response to Listeria monocytogenes (LM) infection. We found that truncating infection and Ag display with antibiotic treatment as early as 24 h postinfection had minimal impact on the expansion or contraction of CD4+ T cells; however, the magnitudes of the Ag-specific CD4+ and CD8+ T cell responses were differentially affected by the timing of antibiotic treatment. Treatment of LM-infected mice with antibiotics at 24 h postinfection did not prevent generation of detectable CD4+ and CD8+ memory T cells at 28 days after infection, vigorous secondary expansion of these memory T cells, or protection against a subsequent LM challenge. These results demonstrate that events within the first few days of infection stimulate CD4+ and CD8+ T cell responses that are capable of carrying out the full program of expansion and contraction to functional memory, independently of prolonged infection or Ag display.

Ampicillin↗

PubMed1994

Role of macrophages and alpha beta T lymphocytes in early interleukin 10 production during Listeria monocytogenes infection.

Immunity to intracellular bacteria including Listeria monocytogenes is determined by Th1 cells and CD8 T cells which produce interferon-gamma. Here we show that high levels of IL-10 are released by splenocytes from mice infected with L. monocytogenes. IL-10 was detected on day 1 after infection, peaked on day 4, and subsequently declined. Cell separation studies and experiments with RAG-1-deficient mice, which do not possess mature B cells or T cells, revealed that the macrophage is the major cellular source of early IL-10 production. Elevated IL-10 production in RAG-1 mutants and TCR beta mutants, but not in TCR delta mutants, is consistent with an inhibition of macrophage IL-10 release by alpha beta T cells. High IL-10 production was also seen after infection with another intracellular bacterium, Mycobacterium bovis. Since IL-10 inhibits Th1 cell responses, certain pathogens might use induction of this cytokine as an evasion mechanism from the protective immune response of the host. However, our findings showing high levels of IL-10 production in infectious models which are dominated by Th1 cell responses suggest that IL-10 alone is insufficient for directing Th0 differentiation into the Th2 cell pathway. These findings therefore challenge the view of IL-10 as a unique and decisive determinator of the Th2 cell pathway.

Animals↗

PubMed1999

Noncompetitive expansion of cytotoxic T lymphocytes specific for different antigens during bacterial infection.

Listeria monocytogenes is an intracellular bacterium that elicits complex cytotoxic T-lymphocyte (CTL) responses in infected mice. The responses of CTL populations that differ in antigen specificity range in magnitude from large, dominant responses to small, subdominant responses. To test the hypothesis that dominant T-cell responses inhibit subdominant responses, we eliminated the two dominant epitopes of L. monocytogenes by anchor residue mutagenesis and measured the T-cell responses to the remaining subdominant epitopes. Surprisingly, the loss of dominant T-cell responses did not enhance subdominant responses. While mice immunized with bacteria lacking dominant epitopes developed L. monocytogenes-specific immunity, their ability to respond to dominant epitopes upon rechallenge with wild-type bacteria was markedly diminished. Recall responses in mice immunized with wild-type or epitope-deficient L. monocytogenes showed that antigen presentation during recall infection is sufficient for activating memory cells yet insufficient for optimal priming of naive T lymphocytes. Our findings suggest that T-cell priming to different epitopes during L. monocytogenes infection is not competitive. Rather, T-cell populations specific for different antigens but the same pathogen expand independently.

Animals↗

PubMed2002

Effects of Chlorella vulgaris extract on cytokines production in Listeria monocytogenes infected mice.

In this study, we have investigated the effects of the unicellular-green-algae Chlorella vulgaris on the production of INF-gamma, IL-2, IL-4 and IL-10 in normal and Listeria monocytogenes infected mice. Our results demonstrated that in normal/non infected mice, CVE administration produced no effects in the levels of all cytokines studied. However, Listeria monocytogenes infection enhanced the production of INF-gamma and IL-2 at 48 and 72 h after the bacteria inoculation. Interestingly, the treatment with five consecutive doses of 50 mg/Kg/day of Chlorella vulgaris given previously to infection, led to further increases in INF-gamma and IL-2 levels at 48 and 72 h in relation to the presence of infection alone. No changes in IL-4 and IL-10 production were observed in Listeria monocytogenes and CVE treated/infected mice. These results are in accordance with the literature, which shows that CVE is a biological response modifier that enhances resistance to Listeria monocytogenes through augmentation of IL-2 and IFN-gamma.

Animals↗

PubMed1988

Protective effect of a traditional Chinese medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to), on Listeria monocytogenes infection in mice.

Lethal effect of Listeria monocytogenes (L. monocytogenes) in mice was prevented by an intraperitoneal (ip) injection of a traditional Chinese herbal medicine, xiao-chai-hu-tang (Japanese name: shosaiko-to), 4 days before ip bacterial infection. The numbers of bacteria in the peritoneal cavity and liver were smaller in shosaiko-to-treated mice from one day after the infection. Macrophage accumulation in the peritoneal cavity after ip inoculation of L. monocytogenes was observed in both untreated and shosaiko-to-treated mice. Although rates of such increases were almost the same between both groups, the absolute number of macrophages was larger in shosaiko-to-treated than in untreated mice because of a higher level of the macrophage number at 4 days after ip injection of shosaiko-to. In untreated mice, bactericidal activity of peritoneal macrophages decreased from one day to 3 days after ip injection of killed L. monocytogenes. Such an activity was maintained at the same level from 1 to 3 days in shosaiko-to-treated mice. Augmented accumulation of macrophages and maintenance of their bactericidal activity may be main mechanisms of the augmented resistance in shosaiko-to-treated mice. Augmented resistance against bacterial growth in the thigh muscle in ip shosaiko-to-treated mice may be caused by such mechanisms. The effect of shosaiko-to observed at an early stage of infection may be T cell-independent, since such an effect was observed in athymic nude mice and delayed footpad reaction could not be detected at such a timing in euthymic normal mice.

Animals↗