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PubMed1998

Host cell signalling during Listeria monocytogenes infection.

Macrophages and other mammalian cells respond to infection with Listeria 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, some of which may hinder or favour bacterial replication. The observed host cell responses vary with the different subcellular locations inhabited by L. monocytogenes during its intracellular life cycle.

Animals↗

PubMed1986

Augmented induction of interferons during Listeria monocytogenes infection.

Mice infected iv with an immunizing dose of the gram-positive bacterium, Listeria monocytogenes, produced circulating interferon (IFN) during the inductive phase of the immune response to Listeria. Listeria infection also dramatically altered the host's responsiveness to IFN-inducing agents. Within 24 hr of infection, mice acquired a 50-fold greater than normal capacity to produce the IFN alpha and/or IFN beta classes (IFN alpha/beta) following iv injection of endotoxin. Serum levels of IFN alpha/beta peaked by 2 hr, after which high levels of IFN gamma were detected in the sera of Listeria-infected mice given the B cell mitogen. Similar studies carried out with the interferon-inducing agent polyinosinic-polycytidylic acid (poly(I).poly(C) revealed that mice infected for 24 hr produced only 4-8 times more IFN alpha/beta than did noninfected mice. Unlike endotoxin, however, poly(I).poly(C) did not induce IFN gamma in Listeria-infected animals.

Animals↗

PubMed1999

MHC class Jb-restricted cell responses to Listeria monocytogenes infection.

Murine infection with Listeria monocytogenes induces CD8+ T cell responses specific for bacterial peptides that are presented on the infected cell surface by MHC class Ia and MHC class Ib molecules. We have used MHC tetramers to demonstrate that CD8+ T cells restricted by the H2-M3 MHC class Ib molecules constitute a substantial portion of the T cell response to L. monocytogenes infection. The in vivo size and kinetics of MHC class Ib-restricted T cell populations suggests that they play a prominent role in bacterial clearance following primary L. monocytogenes infection.

Animals↗

PubMed2000

Differences in interleukin-12 and -15 production by dendritic cells at the early stage of Listeria monocytogenes infection between BALB/c and C57 BL/6 mice.

The mechanisms responsible for the resistance of C57BL/6 mice and for the susceptibility of BALB/c mice to infection with Listeria monocytogenes were studied by comparing early IL-12 and IL-15 production by dendritic cells (DC) after infection with L. monocytogenes. Splenic DC expressing CD11b(low) and CD11c(+) obtained from C57BL/6 mice at 3 and 6 h after L. monocytogenes infection expressed higher levels of IL-12 p40 mRNA and IL-12 p40 protein than did those from BALB/c mice. Concurrently, a larger amount of IFN-gamma was produced by the splenic T cells from C57BL/6 mice in response to immobilized anti-TCRalphabeta mAb than by those from BALB/c mice, while the splenic T cells from BALB/c mice produced a higher level of IL-4 upon TCR alphabeta stimulation than did those of C57BL/6 mice. IL-15 mRNA and intracellular IL-15 protein were detected more abundantly in the DC from C57BL/6 mice than in those from BALB/c mice on day 3 after infection. CD3(+) IL2Rbeta (+) cells in the spleen were increased in C57BL/6 mice but not in BALB/c mice at the early stage after infection. Furthermore, IL-12Rbeta2 gene expression was up-regulated in T cells from C57BL/6 mice but not in those from BALB/c mice at the early stage after listerial infection. These results suggest that the difference in early production of IL-12 and IL-15 by DC may at least partly underlie the difference in susceptibility to L. monocytogenes between C57BL/6 and BALB/c mice.

Animals↗

PubMed1989

Interactions between endogenous gamma interferon and tumor necrosis factor in host resistance against primary and secondary Listeria monocytogenes infections.

Intravenous injection of rat anti-mouse gamma interferon (IFN-gamma) monoclonal antibody as well as rabbit anti-mouse tumor necrosis factor (TNF) antibody into mice which had received a sublethal infection with Listeria monocytogenes cells resulted in acceleration of listeriosis. Endogenous IFN-gamma seemed to be produced early in infection, because suppression of antilisterial resistance was significant when a single injection of anti-IFN-gamma monoclonal antibody was given on day 0 or day 1 of infection. Production of TNF but not of IFN-gamma in the bloodstream early in infection was inhibited by administration of anti-IFN-gamma monoclonal antibody. The suppressive effect of anti-IFN-gamma and anti-TNF antibodies on antilisterial resistance was not augmented by simultaneous administration of these antibodies. On the other hand, in the secondary infection, simultaneous administration of anti-IFN-gamma and anti-TNF antibodies, but not of either of these antibodies alone, into L. monocytogenes-immune mice resulted in high mortality and explosive multiplication of bacterial cells in the spleens and livers. These results suggest that endogenously produced IFN-gamma and TNF are both essential to the host defense against L. monocytogenes infection and that these cytokines might act by different modes between the primary infection and the secondary infection.

Animals↗

PubMed2006

The onset of CD8+-T-cell contraction is influenced by the peak of Listeria monocytogenes infection and antigen display.

The CD8+-T-cell response to infection with Listeria monocytogenes consists of expansion, contraction, and memory phases. The transition between expansion and contraction is reported to occur on different days postinfection with virulent (8 to 9 days) and attenuated (DeltaactA) (7 days) L. monocytogenes strains. We hypothesized that differences in the infectious courses, and therefore antigen (Ag) display, determine the precise time of the expansion/contraction transition in response to these infections. To test this, we infected BALB/c mice with 0.1 50% lethal dose of DeltaactA or virulent L. monocytogenes and measured bacterial numbers, Ag display, and Ag-specific CD8+-T-cell responses on various days after infection. We found that bacterial numbers and Ag display peaked between 12 and 36 h and between 36 and 60 h after infection with DeltaactA and virulent L. monocytogenes strains, respectively. Infection with DeltaactA L. monocytogenes resulted in a sharp peak in the Ag-specific CD8+-T-cell response on day 7, while infection with virulent L. monocytogenes yielded a prolonged peak with equivalent numbers of Ag-specific CD8+ T cells on days 6, 7, and 8 after infection. Truncating virulent infection with antibiotics on day 1 or 2 after infection resulted in a shift in the expansion/contraction transition from day 8 to day 7 after infection. However, antibiotic treatment beginning on day 3, after the peak of virulent L. monocytogenes infection and Ag display, had no effect upon the magnitude or timing of the CD8+-T-cell response. These results demonstrate a direct relationship between the course of infection and Ag display and that the timing of these events is important in shaping the T-cell response to infection.

Animals↗

PubMed1997

Immunodominant and subdominant CTL responses to Listeria monocytogenes infection.

Protective immunity to infection by intracellular pathogens begins with expansion of Ag-specific, effector T lymphocytes and is followed by persistence of pathogen-specific memory T cells. Infection by Listeria monocytogenes, an intracellular bacterium, induces cytolytic T lymphocytes that mediate systemic sterilization and long term immunity. In cells infected with L. monocytogenes, H2-Kd class I molecules present three nonamer peptides, listeriolysin (LLO) 91-99, p60 217-225, and p60 449-457, to CTL. Herein we show that during the peak CTL response to L. monocytogenes infection, the ratio of T cells specific for LLO 91-99, p60 217-225, and p60 449-457 is approximately 20:10:1, respectively. While the number of Ag-specific T lymphocytes decreases in the weeks after infection, the proportion of T lymphocytes specific for the three epitopes is maintained. Repertoire analysis of a subset of L. monocytogenes-specific T cells, using alanine-substituted variants of p60 217-225, indicates that the range of T cell specificities is maintained by memory cells. These results indicate that the breadth and relative magnitude of T cell specificities initially elicited by an infection are transmitted to the memory compartment. Our results suggest that T lymphocytes with different gross and fine Ag specificities are equally likely to become memory T cells.

Acute Disease↗

PubMed1988

Endogenous tumor necrosis factor (cachectin) is essential to host resistance against Listeria monocytogenes infection.

During a sublethal murine infection with Listeria monocytogenes cells, tumor necrosis factor (TNF) activity was detectable in neither sera nor spleen homogenates at any stage of the infection when a bioassay with L-929 cells (less than 4 U/ml) was used. However, injecting the mice with an immunoglobulin fraction obtained from a rabbit hyperimmunized with recombinant murine TNF-alpha resulted in acceleration of listeriosis. When 1 mg of anti-TNF antibody was injected per mouse, all the mice died from listeriosis, even though the infectious dose was sublethal for the untreated controls. The antigen-specific elimination of the bacterium from the spleens and livers of anti-TNF antibody-treated mice was delayed, depending on the dose of the antibody injected. Endogenous TNF seemed to be produced early in infection, because suppression of antilisterial resistance was significant when a single injection of anti-TNF antibody was given between day zero and day 2 of infection. The effect of endogenous TNF on antilisterial resistance was due to neither regulation of alpha interferon (IFN-alpha) and IFN-gamma production nor induction of IFN-beta subtype 1 (IFN-beta 1), because anti-TNF antibody treated-mice produced normal levels of IFN-alpha and IFN-gamma in the bloodstream during infection and administration of monoclonal anti-murine IFN-beta 1 antibody had no effect on the development of listeriosis. Alternatively, the listericidal activity of peritoneal macrophages of L. monocytogenes-infected mice could be abrogated by injection of anti-TNF antibody in vivo. These results suggest that the lower level of TNF is produced endogenously in mice that received L. monocytogenes infection and that it plays an essential role in the host defense against L. monocytogenes infection.

Animals↗

PubMed1997

The characterization of testicular cell (TC)-specific T-cell clones induced by intratesticular Listeria monocytogenes infection: TC-specific T cells with atypical cytokine profile transfer orchitis.

A unilateral infection of Listeria monocytogenes into the testis of mice induces not only Listeria-specific T cells but also autoreactive T cells that can transfer experimental autoimmune orchitis (EAO) into naive mice. To investigate the characteristics of the autoreactive T cells, we established six testicular cell (TC)-specific T-cell clones from the spleen of the intratesticularly infected mice. All the clones expressed CD4 and T-cell receptor (TCR) alpha beta, and four of the six clones expressed V beta 8. They showed proliferative response to TC in the presence of syngeneic spleen antigen-presenting cells, but did not cross-react to Listeria antigen (Ag). They produced interferon-gamma (IFN-gamma) when stimulated with TC, but interleukin-2 (IL-2), IL-4 and IL-10 were undetectable. IL-2 production was not detected even when they were restimulated with TC after a 10-day resting culture without Ag and IL-2, although they proliferated in the restimulation culture. Even in the presence of anti-IL-2 mAb, the TC-specific T-cell clones showed proliferative response against TC. The observations indicate that the TC-specific IFN-gamma-producing T cells proliferate in the absence of autocrine. Both intravenous and intratesticular injection of these clones transferred EAO in syngeneic naive mice. These results suggest that L. monocytogenes infection in the testis induces autoreactive orchitogenic CD4+ T cells without cross-reactivity to bacterial Ag. Furthermore, these data demonstrate that CD4+ T cells with an atypical cytokine profile can efficiently cause EAO.

Adoptive Transfer↗

PubMed1999

The antibacterial efficacy of trovafloxacin against an experimental infection with Listeria monocytogenes in hydrocortisone-treated mice.

The efficacy of trovafloxacin in treating Listeria monocytogenes infections in glucocorticosteroid-treated mice was compared with the efficacy of amoxycillin. Swiss mice were treated with daily injections of 2.5 mg hydrocortisone s.c. and then infected i.v. with 1 x 10(7) cfu of L. monocytogenes. Untreated, this level of infection resulted in 100% mortality between day 3 and day 5 after infection. Both s.c. trovafloxacin and amoxycillin were effective in reducing the number of viable L. monocytogenes in the liver and spleen. Although the MIC of amoxycillin for this isolate of L. monocytogenes was lower than that of trovafloxacin (0.063 mg/L versus 0.5 mg/L, respectively), trovafloxacin was more efficacious in vivo after a single dose in the dose range between 12.5 and 100 mg/kg than was amoxycillin. After treatment with trovafloxacin at 100 mg/kg bodyweight od for 3 days, a mean log10 cfu of 1.58 and 2.52 L. monocytogenes could be recovered from the spleens and livers, respectively, whereas after treatment with amoxycillin at 100 mg/kg bodyweight every 8 h for 3 days, the mean 1og10 cfu values were 2.36 and 2.02, respectively. These differences were statistically not significant. Results of the present study show that the antibacterial efficacy of trovafloxacin against L. monocytogenes in our animal model is equivalent to that of amoxycillin.

Amoxicillin↗

PubMed1981

Mechanism for nonspecific immunity of Listeria monocytogenes in rats mediated by platelets and the clotting system.

A proposed mechanism for nonspecific immunity to Listeria monocytogenes in rats based on the existence of an activatable lysin is described. Using a deoxyribonucleic acid release assay, we found lysin activity in serum made from whole blood but not in serum made from platelet-free plasma. Washed platelets and platelet lysates exhibited only partial activity as compared with that in serum. This activity was amplified by the addition of platelet-free plasma serum. The activity of the lysin was unaffected by heparin, dialysis, a serine esterase inhibitor, or heating to 56 degrees C for 30 min. Effective inhibitors were ethylenediaminetetraacetic acid and stronger heating (to 65 degrees C). Listeria organisms were found to reduce the recalcified clotting time to platelet-rich plasma in a dose-dependent fashion, indicating that the organisms can exhibit procoagulant activity. The susceptibility of rats to Listeria infection was enhanced by anticoagulant treatment. Rats were infected with Listeria organisms with and without administration of heparin. Heparin-treated rats developed bacteremia, and some died. None of the control rats developed bacteremia or died. These results suggest that natural immunity to Listeria infection is partly due to a platelet-dependent lysin which is activated during clotting and is, in turn, promoted by the Listeria organisms themselves.

Animals↗

PubMed2003

The role of dietary vitamin E in experimental Listeria monocytogenes infections in turkeys.

The current study was designed to determine if dietary vitamin E influenced either the gut clearance or levels of peripheral blood CD4+ and CD8+ T lymphocytes in adult turkeys experimentally infected with Listeria monocytogenes. Turkeys were fed vitamin E (0, 100, or 200 IU) from day of hatch to time of necropsy. After 6 wk on the experimental diet, turkeys were orally inoculated with L. monocytogenes (approximately 10(9) cfu). To monitor infection status, cloacal swabs were taken on selected days post-inoculation (DPI). At necropsy, samples of viscera, including liver, spleen, cecum, duodenum, ileum, and colon were collected and cultured for L. monocytogenes. In experiments 1 and 2, recovery of L. monocytogenes from cloacal swabs, tissues, and intestines from turkeys fed vitamin E was generally lower than that from turkeys fed the control diet, although these differences were not statistically significant. When data from both trials were combined, L. monocytogenes was cultured less frequently from cloacal swabs of the vitamin E-treated group (200 IU) on 2 and 3 DPI, when compared to controls (0 IU, P < 0.01). There were no changes in virulence characteristics of L. monocytogenes cells, as measured by in vitro killing of Ped-2E9 cells, recovered from cloacal swabs or tissues of experimentally infected turkeys fed the control or a vitamin E treatment diet. Flow cytometric analysis indicated that CD4+ and CD8+ peripheral blood T lymphocytes were elevated at 6 and 8 DPI in infected turkeys given 200 IU vitamin E.

Animals↗

PubMed1995

Polysaccharide (ANK-102) from Polianthes tuberosa cells deteriorates the resistance of mice to Listeria monocytogenes infection.

Modulatory effect on the murine self defense system by a newly discovered acidic polysaccharide (ANK-102) produced by P. tuberosa cells in liquid culture was examined. Pretreatment with ANK-102 deteriorated the murine survival against lethal infection of Listeria monocytogenes, an intracellular gram-positive bacterium eliminated mainly by macrophages through T-cell mediated immune response. Pretreatment with ANK-102 resulted in the accumulation of Mac 1 and Mac 2 positive cells in the peritoneal cavity of the infected animals and the reduction of Thy1.2 expression on the surface of the thymocytes. A new type of immunosuppressive polysaccharide ANK-102 was introduced.

Animals↗

PubMed1972

Mechanisms of pathogenesis in Listeria monocytogenes infection. VI. Oxidative phosphorylation in mouse liver mitochondria during experimental listeriosis.

Previous reports have demonstrated early changes in hepatic carbohydrate and energy metabolism in mice infected with Listeria monocytogenes. This study was undertaken to further elucidate mechanisms of damage involved in these changes. Female CD-1 mice were injected intraperitoneally with 10(6)L. monocytogenes A4413. At 0, 10, and 20 hr after infection, groups of mice were sacrificed and the livers were removed and pooled. Oxidative phosphorylation was assayed immediately upon isolation of mitochondria from pooled liver homogenates. Appropriate metabolic inhibitors were employed to examine each of the three phosphorylation sites in mitochondrial electron transport. When pyruvate-malate (equimolar concentrations) and alpha-ketoglutarate were used as substrates, decreases in both phosphorylation and oxidation were noted as early as 10 hr after infection. With beta-hydroxybutyrate and citrate as substrates, alterations were not noted until 20 hr after infection, whereas no changes were seen when glutamate, succinate, or ascorbate were employed. These results suggest possible derangement of the first site in oxidative phosphorylation as well as lowered activity of nicotinamide adenine dinucleotide-linked dehydrogenases during experimental listeriosis in mice.

Animals↗

PubMed1972

Mechanisms of pathogenesis in Listeria monocytogenes infection. V. Early imbalance in host energy metabolism during experimental listeriosis.

Early changes in hepatic carbohydrate metabolism without apparent hepatocyte dysfunction were reported previously in mice infected with Listeria monocytogenes. This study was undertaken to examine possible imbalance in host regulatory mechanisms which might be responsible for these changes. Female CD-1 mice fasted 12 hr prior to the experiments were injected intraperitoneally with 10(5), 10(6), or 10(7)Listeria. Control mice received either 10(9) heat-killed Listeria or 150 mug of Salmonella typhimurium lipopolysaccharide. Hepatic glycogen, adenosine triphosphate (ATP), adenosine diphosphate (ADP), and nicotinamide adenine dinucleotide (NAD) (NAD(+), NADH, NADP(+), and NADPH) levels were assayed periodically. Activities of ATP hydrolyzing enzyme and NAD glycohydrolase were measured at various intervals after infection. Decreases in glycogen occurred as early as 10 hr after infection. Responses in the controls differed from those in infected mice. Hepatic ATP levels decreased as early as 10 hr after infection, with concomitant increases noted in ADP. Hepatic ATP hydrolyzing enzyme activity increased as the infection progressed. Decreases were noted in hepatic NAD levels, with the greatest reduction in the reduced form of NAD. Slight changes were observed after 10 hr, and greater differences were noted 20 hr after infection. The magnitude of these biochemical changes appeared to be dose-dependent. Significant increases in hepatic NAD glycohydrolase activity were noted as the infection progressed. Small but significant increases in serum inorganic phosphate were noted 10 and 20 hr after infection, with a larger increase observed 30 hr after infection. The results indicate impairment of host energy metabolism early in the course of experimental listeriosis.

Adenosine Diphosphate↗

PubMed2003

Anti-oxidant properties of N-acetyl-L-cysteine do not improve the immune resistance of mice fed dietary lipids to Listeria monocytogenes infection.

BACKGROUND & AIMS: Current knowledge of the potential effects that several dietary lipids exert on immune functions indicates that these substances participate actively in the modulation of immune system by which they contribute to the improvement of the conditions of patients suffering from inflammatory disorders. However, long-chain n-3 polyunsaturated fatty acids induce an immunosuppressive status that leads to a reduction of the host natural resistance to infectious agents as well as to an enhancement of oxidative damage. Hence, the present study has been designed to evaluate the effects on the immune system of the antioxidant N-acetyl-L-cysteine (NAC) in mice fed dietary lipids and infected with Listeria monocytogenes. METHODS: Balb/c mice were fed for 4 weeks with diets containing either olive oil (OO, 20% by weight), fish oil (FO, 20% by weight) or hydrogenated coconut oil (HCO, 20% by weight). After dietary lipid administration mice were experimentally infected with L. monocytogenes or treated with NAC (25mg/ml intraperitoneally). RESULTS: NAC at a concentration of 1mM promoted a loss of cell viability, although no differences were observed among the four groups. After injection of NAC in combination with L. monocytogenes, 25% of mice fed a low-fat (LF) diet survived. However, in the groups fed dietary lipids no effect on survival of mice was found. NAC participated in the reduction of superoxide anion generation measured with nitroblue tetrazolium (NBT) in the group fed a FO diet. Finally, NAC reduced the recovery of L. monocytogenes from spleen of mice fed diets containing LF or HCO. CONCLUSIONS: On the basis of these results, we can confirm that the administration of NAC improves survival in mice fed LF diet, whereas a reduction in the generation of superoxide radicals was measured in mice fed a FO diet and infected with L. monocytogenes. Similarly, bacterial recovery was diminished in mice fed diets containing LF or HCO. Hence, these data reveal a beneficial effect of NAC in mice fed LF or HCO and a detrimental action of this antioxidant in mice fed diets containing FO or OO.

Acetylcysteine↗

PubMed2002

Neonatal lead exposure potentiates sickness behavior induced by Listeria monocytogenes infection of mice.

The effects of lead (Pb) administration on infection-induced decreases in water intake, food intake, and body weight gain have been assessed as manifestations of sickness behavior using a BALB/c mouse model. Pb acetate (0.5 mM) was administered via drinking water to dams from Day 0 postpartum to weaning and to mouse pups after weaning until sacrifice. At 22 days after birth, young mice were infected with Listeria monocytogenes. Mice with blood Pb levels of less than 25 microg/dl exhibited enhanced and prolonged sickness behavior compared to mice not exposed to Pb. With this mouse model, after infection, serum levels of interleukin (IL)-1beta and IL-6 were enhanced in Pb-exposed mice. Compared with control infected mice, significant reductions in the number of thymic CD4(+)CD8(+), CD4(+), CD8(+), and CD4(-)CD8(-) T cells were observed in Pb-exposed mice. As a substitute for the infection, mice were injected with IL-1 and/or IL-6; Pb exacerbated sickness behavior only in mice injected peripherally with IL-1 and IL-6. Our data in young mice suggest that children with blood Pb levels during bacterial infection may exhibit enhanced and prolonged sickness behavior due to Pb/cytokine-dependent processes and that Pb appears to influence sickness behavior depending on the types and amounts of cytokines generated.

Animals↗

PubMed1970

Mechanisms of Pathogenesis in Listeria monocytogenes Infection IV. Hepatic Carbohydrate Metabolism and Function in Experimental Listeriosis.

Previous reports have shown alterations in carbohydrate metabolism in mice infected with Listeria monocytogenes. This study was undertaken to elucidate mechanisms involved in these changes. Female CD-1 mice were injected intraperitoneally with 10(6)L. monocytogenes strain A4413. Animals were fasted 12 hr prior to infection, and pooled tissue from several mice was observed at intervals after infection. Blood glucose, liver glucose, and liver glycogen decreased within 10 hr after infection. Sustained treatment with gluconeogenic precursors, including glucose-6-phosphate, fructose-1, 6-biphosphate, phosphoenolpyruvate, alpha-glycerophosphate, pyruvate, and amino acids, did not restore and maintain glucose and glycogen at normal levels and did not affect survival. Administration of hydrocortisone induced restoration of liver glycogen early in the infection but did not maintain normal levels as the infection progressed. Activities of succinic dehydrogenase and cytochrome oxidase in liver homogenates from infected mice were elevated as early as 10 hr after infection. Liver function tests using rose bengal sodium-(131)I showed no significant differences in plasma clearance or liver uptake between normal and infected mice except in terminal infections (60 hr after infection).

Journal Article↗