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PubMed1976

[Bacteriological and pathohistological studies of sheep experimentally infected with Listeria].

A total of forty gimmers (eight of which spleen-ectomized) were i/v, orally, intratracheally, and along the branching of n. infraorbitalis infected with a 24-hour broth culture of Listeria monocytogenes. The meningoencephalite form of listeriosis was induced in two of the animals infected intraveneously, in one animal of those infected orally, and in one of those infected in the branching of nervus infraorbitalis. The most typical microscopic changes were established in the case of infection through the veins and the nerves. It was concluded that these were probably the most often occurring ways of infection and dissemination of Listeria. However, the resistance of the host organism, the number of bacteria, and the virulence were also of interest. Toxic injury of the brain and the viscera of all infected sheep were also found.

Animals↗
PubMed2003

In vitro study of Listeria monocytogenes infection to murine primary and human transformed B cells.

Immunity to Listeria monocytogenes is largely mediated by T lymphocytes. Recently, B lymphocytes or their secreted products are implicated to provide immunity against L. monocytogenes infection. To understand whether L. monocytogenes can infect and kill B cells as a possible strategy to initiate an infection, we examined the effects of L. monocytogenes on a human B lymphoma (Ramos RA-1) and mouse primary B cells in vitro. L. monocytogenes infection resulted in significantly (p<or=0.05) high cytotoxicity (58-79%) for Ramos and 39-68% cytotoxicity for mouse primary B cells. In contrast, non-pathogenic L. innocua caused only 1.2% cytotoxicity for Ramos and 19% for primary B cells. Bacterial cells were found frequently adhered to the B cell surfaces; however, active invasion was not a prerequisite for infection. L. monocytogenes caused loss of B cell surface molecules, pore formations, cell swelling, membrane damages and apoptosis. This study demonstrates that L. monocytogenes can infect and kill B cells as a possible strategy to initiate a successful infection.

Animals↗
PubMed1995

Influence of steric stabilization of liposome-encapsulated hemoglobin on Listeria monocytogenes host defense.

Liposome-encapsulated hemoglobin (LEH) products are being investigated as potential blood substitutes. To determine if changes in LEH composition can modify the immune response, red blood cell substitutes based on conventional lipids containing phosphatidylinositol (LEH1) and sterically stabilized lipid vesicles containing polyethylene glycol phosphatidylethanolamine (LEH2) were tested for effects on host resistance. On Day 0, groups of 18 to 20 female CD-1 mice were given an intravenous (i.v.) infectious challenge with a 20% lethal dose of Listeria monocytogenes. Mice received a single i.v. dose of LEH1, LEH2, or albumin vehicle on Day +1 or Day -3 relative to infectious challenge. Mice dosed with LEH1 and LEH2 on Day +1 died rapidly from Listeria infection; but mice dosed with LEH2 lived significantly longer than did mice receiving LEH1. By contrast, when administered on Day -3, LEH1 had no significant effect on host immunity, while LEH2 increased susceptibility to Listeria infection. In addition, LEH1 and LEH2 both caused significant reduction of phagocytic activity as measured by rat alveolar macrophage (AM) ingestion of latex microspheres. AM incubated 4 hr with either LEH1 or LEH2 prior to addition of microspheres ingested fewer beads in a dose-dependent manner. No difference in in vitro phagocytic activity was observed between LEH1 or LEH2. The inability to differentiate LEH formulations based on in vitro phagocytic activity suggests that the in vivo Listeria infection model may be more relevant in discerning the immunotoxicity of the LEH formulations tested.

Animals↗
PubMed2002

Mitogen-activated protein kinase-activated protein kinase 2-deficient mice show increased susceptibility to Listeria monocytogenes infection.

Mitogen-activated protein kinase-activated protein kinase 2 (MK2) is one of several kinases activated through direct phosphorylation by p38 mitogen-activated protein kinase. MK2 regulates LPS-induced TNF mRNA translation, and targeted mutation of the MK2 gene renders mice more resistant to D-galactosamine plus LPS-induced liver damage. In the present study, we investigated the role of MK2 in immune defense against Listeria monocytogenes infection. MK2-deficient mice displayed diminished resistance to L. monocytogenes due to impaired control of bacterial growth. The increase in bacterial load in MK2(-/-) mice was associated with normal levels of IL-1 beta, IL-6, and IFN-gamma, whereas TNF production was strongly attenuated. In line, MK2-deficient bone marrow-derived macrophages showed impaired release of TNF, but not of IL-1 beta, in response to various bacterial stimuli in addition to decreased phagocytosis of fluorescence-labeled bacteria. Furthermore, spleen cells from MK2(-/-) mice displayed diminished IFN-gamma synthesis after stimulation with L. monocytogenes. In contrast, MK2 deficiency had no effect on macrophage generation of NO or on oxidative burst activity in response to L. moocytogenes. These results indicate an essential role of MK2 in host defense against intracellular bacteria probably via regulation of TNF and IFN-gamma production required for activation of antibacterial effector mechanisms.

Animals↗
PubMed1971

Rapid method for the isolation of Listeria monocytogenes from experimentally infected mice.

Listeria monocytogenes was successfully isolated from experimentally infected mice by placing homogenized tissues in phosphate-buffered saline (PBS), trypsin, peptone, or pepsin followed by incubation at 37 C for 24 hr. A larger number of Listeria isolates were recovered from the trypsin or PBS splenic homogenate suspensions incubated at 37 C for 2 hr than from the other diluent suspensions. Holding infected tissues at 4 C for at least 3 months did not increase the efficiency of Listeria isolation. Listeria L-forms were not isolated from mice injected with the bacterial form. The in vitro viability of Listeria L-forms suspended in PBS or PBS splenic homogenate was greatly reduced when held at 4 C.

Agar↗
PubMed1992

Endogenous tumor necrosis factor, interleukin-6, and gamma interferon levels during Listeria monocytogenes infection in mice.

Mice were infected intravenously with a sublethal dose of Listeria monocytogenes cells and then levels of tumor necrosis factor (TNF), interleukin-6 (IL-6), and gamma interferon (IFN-gamma) in the bloodstreams, spleens, and livers were monitored. The maximum level of TNF was detected at 72 h in the spleens and livers, but TNF was never detected in the bloodstreams. IL-6 appeared in the bloodstreams and spleens and peaked at 48 h. The maximum level of IFN-gamma could be detected in all three specimens, and the highest titer was shown in the spleens. Endogenous TNF production was suppressed by in vivo administration of anti-CD4 monoclonal antibody (MAb) or anti-asialo GM1 antibody but not by anti-CD8 MAb, whereas none of these antibodies suppressed endogenous IL-6 production. Endogenous production of neither IL-6 nor IFN-gamma was inhibited in rabbit anti-recombinant mouse TNF-alpha antibody-treated mice. Similarly, production of TNF and IL-6 did not decrease in anti-mouse IFN-gamma MAb-treated animals, but TNF production was augmented in these animals. These results suggest that the these endogenous cytokines are produced by different mechanisms in L. monocytogenes infection.

Animals↗
PubMed2000

Effect of a matrix metalloproteinase inhibitor on host resistance against Listeria monocytogenes infection.

Hydroxy acid-based matrix metalloproteinase (MMP) inhibitors have been shown to inhibit tumor infiltration and growth, endotoxin shock, and acute graft-versus-host disease. Blockade of the release of soluble tumor necrosis factor-alpha (TNF-alpha) and CD95 ligand (CD95L; FasL) from cell-associated forms is reportedly involved in the mechanism of the drug effect. We investigated the effect of a MMP inhibitor, KB-R7785, on host resistance against Listeria monocytogenes infection, in which TNF-alpha is essentially required for the defense, in mice. The administration of KB-R7785 exacerbated listeriosis, while the drug prevented lethal shock induced by lipopolysaccharide and D-galactosamine. KB-R7785 inhibited soluble TNF-alpha production in spleen cell cultures stimulated by heat-killed L. monocytogenes and the drug treatment reduced serum TNF-alpha levels in infected mice, whereas the compound was ineffective on the modulation of interferon-gamma and interleukin-10 production. The effect of KB-R7785 was considered to be dependent on TNF-alpha because the drug failed to affect L. monocytogenes infection in anti-TNF-alpha monoclonal antibody-treated mice and TNF-alpha knockout mice. Anti-CD95L monoclonal antibody was also ineffective on the infection. These results suggest that induction of infectious diseases, to which TNF-alpha is critical in host resistance, should be considered in MMP inhibitor-treated hosts.

Animals↗
PubMed1989

[Four cases of adult Listeria monocytogenes infection in the last 5 years--hepatic necrotic foci in the adult septic case].

We have reported on the clinical courses of 4 cases of adult Listeria monocytogenes (Lm) infection, and the autopsy findings of 2 cases, those we have observed over the past 5 years. They were 2 cases of meningitis, 1 case of meningitis and sepsis and 1 case of sepsis. These 4 cases had CML, neoplastic angioendotheliosis, SLE and post-renal transplant condition, as their underlying diseases, and all were receiving immunosuppressive therapy. One meningitis patient who recovered showed mild liver dysfunction during her clinical course. The other 3 patients who died had jaundice at the time of onset and severe liver dysfunction. The 2 cases those were autopsied were the sepsis cases. The one with an acute course and hepatic failure showed multiple miliary necrotic foci in the liver, where the presence of Lm in the cells could be verified. The other autopsy case, which had received adequate antibiotic therapy and the Lm infection had been cured, showed no necrotic foci in the liver. The case that had necrotic foci in the liver was the first such adult case in Japan. We have discussed the hepatic Lm infection in adult compromised hosts, which conventionally has not been considered a serious problem.

Aged↗
PubMed1996

Effect of multiplicity of infection on Listeria monocytogenes pathogenicity for HeLa and Caco-2 cell lines.

The significance of multiplicity of infection (moi) for invasiveness and intracellular multiplication of Listeria monocytogenes in Caco-2 and HeLa cell monolayers was investigated. A low moi (1:1) resulted in recovery of significantly more L. monocytogenes when these bacteria were used to infect either cell line. At high moi (100:1), the percentage recovery of bacteria was comparatively low, even after extensive invasion and intracellular multiplication. Microscopic analysis of Giemsa- and immunofluorescent-stained infected monolayers revealed extensive cell disruption and exposure of the internalised bacteria to the bactericidal effect of gentamicin. By contrast, a low moi resulted in minimal cytopathic effects and evidence of cell to cell spread by L. monocytogenes was consistently observed in HeLa and J774, but not in Caco-2 cell lines. Nevertheless, the use of HeLa and Caco-2 cell monolayers enabled a clear distinction to be made between invasive (L. monocytogenes) and non-invasive Listeria spp. (L. innocua, L. ivanovii, L. seeligeri, L. grayi, L. welshimeri and L. monocytogenes LLO19). The use of a low moi with HeLa cell monolayers provided a reliable tissue-culture model of infection for L. monocytogenes.

Caco-2 Cells↗
PubMed1989

Spectrum and outcome of microbiologically documented listeria monocytogenes infections in cancer patients.

At the M.D. Anderson Cancer Center (Houston), Listeria monocytogenes was cultured from 14 patients between 1980 and 1987. The case records of 11 of these patients were reviewed. Underlying malignancies included acute leukemia (three), lymphoma (two), myeloma (one), adenocarcinoma of colon (two), carcinoma of breast (one), carcinoma of lung (one), and Kaposi's sarcoma associated with the acquired immune deficiency syndrome (one). Listeria monocytogenes was cultured from blood (eight patients), cerebrospinal fluid (CSF) (two patients), and from both blood and CSF in one patient. All patients were receiving immunosuppressive therapy including corticosteroids in seven. An absolute neutrophil count of less than 1000/mm3 was noted in five. Bacteremia was the predominant type of infection and ten patients responded to antimicrobial therapy.

Adult↗
PubMed1996

Treatment with the antigranulocyte monoclonal antibody RB6-8C5 impairs resistance of mice to gastrointestinal infection with Listeria monocytogenes.

Treatment with the antigranulocyte monoclonal antibody (MAb) RB6-8C5 increased the severity of infection in mice intragastrically inoculated with Listeria monocytogenes. Most MAb RB6-8C5-treated mice died when inoculated intragastrically with as few as 4 x 10(4) L. monocytogenes bacteria, whereas most control mice survived intragastric inoculation with 4 x 10(8) L. monocytogenes bacteria. The increased severity of infection in MAb RB6-8C5-treated mice appeared to result from listerial multiplication in the spleen and liver rather than from local proliferation in the intestinal tract or mesenteric lymph nodes.

Animals↗
PubMed1963

Listeria monocytogenes infections in Metropolitan Toronto. A clinicopathological study.

The clinical and laboratory findings in 21 patients with listeriosis are described and the subject is reviewed. Eleven of the infections were septicemias of newborns, eight were meningitis in infants or adults, and two other children had unusual manifestations.Neonatal septicemia was rapidly fatal; one of 11 infants survived. The disease often seemed traceable to mild maternal infection during the third trimester usually leading to premature delivery of critically ill babies. Only awareness of the possible presence of listeriosis and early antibiotic therapy seem capable of reducing this high mortality.Tissues from autopsies showed characteristic microscopic necrotic foci with mononuclear infiltration progressing to microabscesses containing small Gram-positive rods. Lesions were found in the one placenta examined.Five infants with meningitis recovered, and one of three affected adults. Specific diagnosis depends on demonstrating Listeria monocytogenes; differentiation from other forms of acute meningitis cannot be made clinically.One older child had septicemia and another had listerial pharyngitis. Both recovered.

Abscess↗
PubMed2002

The cell biology of Listeria monocytogenes infection: the intersection of bacterial pathogenesis and cell-mediated immunity.

Listeria monocytogenes has emerged as a remarkably tractable pathogen to dissect basic aspects of cell biology, intracellular pathogenesis, and innate and acquired immunity. In order to maintain its intracellular lifestyle, L. monocytogenes has evolved a number of mechanisms to exploit host processes to grow and spread cell to cell without damaging the host cell. The pore-forming protein listeriolysin O mediates escape from host vacuoles and utilizes multiple fail-safe mechanisms to avoid causing toxicity to infected cells. Once in the cytosol, the L. monocytogenes ActA protein recruits host cell Arp2/3 complexes and enabled/vasodilator-stimulated phosphoprotein family members to mediate efficient actin-based motility, thereby propelling the bacteria into neighboring cells. Alteration in any of these processes dramatically reduces the ability of the bacteria to establish a productive infection in vivo.

Actins↗
PubMed2004

Eye infections due to Listeria monocytogenes in three cows and one horse.

A retrospective study was conducted to determine case histories, microbiological characteristics, and molecular subtypes associated with Listeria monocytogenes infections of the eye in large animals. For selected cases, environmental L. monocytogenes contamination patterns on case farms were also evaluated to probe for potential sources and spread of listerial eye infections. Records of 170 L. monocytogenes isolates from animal infections were reviewed to determine the fraction of isolates associated with eye infections (conjunctivitis, keratitis, and uveitis) of animals and to gather information on the clinical history of these cases. Overall, 4 of 170 Listeria monocytogenes isolates were associated with eye infections; 3 of these had occurred in cows and 1 in a horse. Molecular subtyping (by EcoRI ribotying) showed that 4 different L. monocytogenes subtypes were isolated from these 4 cases; the same ribotypes had previously been found among invasive animal listeriosis infections. Although a variety of L. monocytogenes subtypes were isolated from environmental sources, on 1 farm, the same ribotype associated with the eye infection was also isolated from a fecal sample of a healthy animal and from a soil sample. The data reported in this study further suggest that L. monocytogenes can be a cause of eye infections in several animal species. Listerial eye infections do not seem to require specific pathogen-related virulence characteristics but rather seem to be a function of environmental or host factors, such as direct exposure of the eyes of susceptible animals to high numbers of the pathogen. Although listerial eye infections are rarely diagnosed because of its ubiquitous nature, L. monocytogenes may have to be considered more commonly as a causative agent of eye infections in ruminants and horses.

Animals↗
PubMed2005

Listeriolysin O-induced membrane permeation mediates persistent interleukin-6 production in Caco-2 cells during Listeria monocytogenes infection in vitro.

Listeriolysin O (LLO), a major virulence factor of Listeria monocytogenes, is a member of the cholesterol-dependent cytolysin family and plays important roles not only in survival of this bacterium in phagocytes but also in induction of various cellular responses, including cytokine production. In this work, we examined the involvement of LLO in induction of the cytokine response in intestinal epithelial cells, the front line of host defense against food-borne listeriosis. Infection of Caco-2 cells with wild-type L. monocytogenes induced persistent expression of interleukin-6 (IL-6) mRNA. In contrast, IL-6 expression was observed only transiently during infection with non-LLO-producing strains. A sublytic dose of recombinant LLO (rLLO) induced the expression of IL-6 via formation of membrane pores. Under conditions of LLO-induced pore formation without extensive cell lysis, Ca2+ influx was observed, and the IL-6 expression induced by rLLO was inhibited by pretreatment with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl ester) (BAPTA-AM), an intracellular Ca2+ chelator. LLO secreted by cytoplasmic L. monocytogenes appeared to induce pore formation in the membrane and to enable the trafficking of intracellular and extracellular molecules. Pretreatment with BAPTA-AM inhibited persistent IL-6 expression in Caco-2 cells infected with wild-type L. monocytogenes. These results suggest that LLO is involved in IL-6 production in the late phase of infection through the formation of Ca2+-permeable pores and subsequent Ca2+-dependent modulation of signaling and gene expression.

Bacterial Toxins↗
PubMed1986

Aspects of the epidemiology of human Listeria monocytogenes infections in Britain 1967-1984; the use of serotyping and phage typing.

Strains of Listeria monocytogenes from 475 cases of human listeriosis collected during 1967-1984, belonged to one of three serogroups (1/2, 3 or 4). They were phage typed with a set of 28 phages to investigate three aspects of the epidemiology of listeriosis. Three patients each had two episodes of listeriosis, 3 months to 2 years apart, with strains of the same serogroup and indistinguishable by phage typing. Ten episodes of possible cross-infection between pairs of neonates in the same hospital occurred; the first baby was ill at or within 1 day of birth, and the second baby became ill 8-12 days after contact with the first. In each pair the L. monocytogenes strains were of the same serogroup and indistinguishable by phage typing. In three clusters of cases there may have been a common source of infection. L. monocytogenes strains from 10 of 11 cases of listeriosis in the Carlisle area in Jul.-Dec. 1981 were of the same serogroup; nine strains were non-phage-typable. The second cluster involved four adults treated at one hospital and the third a pair of neonates who were ill shortly after birth. In each cluster, strains were of the same serogroup, and were indistinguishable by phage typing. These last two clusters occurred during a short period when an unusually high proportion of strains from all cases of human listeriosis in Britain were indistinguishable by phage typing from the cluster strains, suggesting the possibility of common source infection.

Adult↗
PubMed1997

Active catabolism of glucocorticoids by 11 beta-hydroxysteroid dehydrogenase in vivo is a necessary requirement for natural resistance to infection with Listeria monocytogenes.

The results from the present study demonstrate that the innate defense mechanisms which control the progressive growth of Listeria monocytogenes in normal animals in vivo are dependent upon the active catabolism of endogenous glucocorticoids by the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD). When 11 beta-HSD activity was pharmacologically inhibited in vivo, host susceptibility to progressive bacterial disease was markedly increased. Depressed natural resistance following 11 beta-HSD inhibition correlated with changes in the patterns of inducible cytokines by macrophages and T cells. Similar changes were observed when normal adult animals were treated with low doses of dexamethasone prior to experimental infection with Listeria.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2003

Indoleamine 2,3-dioxygenase is regulated by IFN-gamma in the mouse placenta during Listeria monocytogenes infection.

The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) is expressed in macrophages that have been differentiated in the presence of CSF-1 and is important in the containment of intracellular pathogens. IDO also appears to play a role in suppression of T cell responses in a variety of contexts. In the placenta, its enzymatic activity is believed to establish a chemical barrier that protects the fetal allograft from T cell-mediated immune aggression. We have studied the regulation of IDO in the utero-placental unit of mice following infection with the Gram-positive, intracellular bacterium Listeria monocytogenes that has a predilection for replication in the decidua basalis. IDO mRNA and protein expression is enhanced in the utero-placental unit following infection with L. monocytogenes. However, in contrast to the human where IDO is expressed by the CSF-1R-positive syncytial trophoblast, IDO is not expressed in murine trophoblastic tissue but instead is found in stromal cells of the decidua basalis and metrial gland and following infection, in endothelial cells. Using mice carrying null mutations in cytokine/growth factor genes, we explored the regulation of IDO in the placenta. Consistent with the absence of CSF-1R expression in the IDO-expressing cells of mice, neither the basal levels of IDO nor its induction following infection is affected by the absence of CSF-1. However, although the basal level of IDO is normal, the enhanced expression during Listeriosis is completely abrogated in the absence of IFN-gamma, a cytokine required for the resolution of this infection. These data suggest that IDO plays a role in resolving bacterial infection in the placenta while at the same time maintaining a barrier to T cells whose presence might result in fetal rejection.

Animals↗