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PubMed1995

The induction of renal autoantigen-specific T cells by a local Listeria monocytogenes infection.

In order to examine the possibility that a local chronic infection can induce organ-specific autoimmune disease, we inoculated unilateral kidneys with viable Listeria monocytogenes (intrarenal infection). The delayed footpad reaction against syngeneic kidney homogenate (KH) became positive from 1 week after initiating the intrarenal infection. A proliferative response of the spleen T cells from the infected mice was also observed against KH from 1 week after initiating the intrarenal infection, but no such response was seen against liver homogenate (LH). In contrast, an intravenous Listeria infection did not induce a delayed footpad reaction or proliferative response against KH, suggesting that these autoimmune responses were not caused by molecular mimicry between renal antigens and Listeria antigens. Furthermore, the ability to transfer the autoimmune response of spleen T cells from intrarenally infected mice was examined. The transferred mice showed a positive delayed footpad reaction against KH and an interstitial infiltration of mononuclear cells in their kidneys. These results demonstrate that the intrarenal Listeria infection induced renal autoantigen-specific T cells, which subsequently induced an autoimmune interstitial nephritis (AIN). The autoreactive T cells were all induced without immunization by autoantigens mixed with complete Freund's adjuvant. Based on these findings, we propose that a local bacterial infection may induce an autoimmune response against autoantigens in the infected organ and subsequently trigger organ-specific autoimmune disease.

Animals↗
PubMed2003

Protective effects of Chlorella vulgaris in lead-exposed mice infected with Listeria monocytogenes.

Chlorella vulgaris extract (CVE) was examined for its chelating effects on the myelosuppression induced by lead in Listeria monocytogenes-infected mice. The reduction in the number of bone marrow granulocyte-macrophage progenitors (CFU-GM) observed after the infection was more severe in the groups previously exposed to lead. Extramedullar hematopoiesis, which was drastically increased after the infection, was not altered by the presence of lead. Treatment with CVE, given simultaneously or following lead exposure, restored to control values the myelosuppression observed in infected/lead-exposed mice and produced a significant increase in serum colony-stimulating activity. The benefits of the CVE treatment were also evident in the recovery of thymus weight, since the reduction produced by the infection was further potentiated by lead exposure. The efficacy of CVE was evident when infected and infected/lead-exposed mice were challenged with a lethal dose of L. monocytogenes after a 10-day treatment with 50 mg/kg CVE/day, given simultaneously to the exposure to 1300 ppm lead acetate in drinking water. Survival rates of 30% for the infected group and of 20% for the infected/lead-exposed groups were observed. Evidence that these protective effects of CVE are partly due to its chelating effect was given by the changes observed in blood lead levels. We have observed in the group receiving the CVE/lead simultaneous exposure a dramatic reduction of 66.03% in blood lead levels, when compared to lead-exposed nontreated control. On the other hand, CVE treatment following lead exposure produced a much less effective chelating effect. CVE treatments for 3 or 10 days, starting 24 h following lead exposure, produced a reduction in blood lead levels of 13.5% and 17%, respectively, compared to lead-exposed nontreated controls. The significantly better response observed with the simultaneous CVE/lead administration indicates that the immunomodulation effect of CVE plays an important role in the ability of this algae to reduce blood lead levels. In this regard, additional experiments with gene knockout C57BL/6 mice lacking a functional IFN-gamma gene demonstrated that this cytokine is of paramount importance in the protection afforded by CVE. The antibacterial evaluation measured by the rate of survival demonstrated that, in face of a 100% survival in the control group composed of normal C57BL/6 mice, which are resistant to L. monocytogenes, we observed no protection whatsoever in the IFN-gamma knockout C57BL/6 mice treated with CVE and inoculated with L. monocytogenes.

Animals↗
PubMed1996

The role of p56lck in the development of gamma delta T cells and their function during an infection by Listeria monocytogenes.

We investigated roles of p56lck tyrosine kinase (Lck) on the development and function of gamma delta T cells in adult mice using lck gene knockout (lck -/-) mice. The mature gamma delta T cells (heat-stable Ag negative) were generated significantly in the thymi of adult lck -/- mice. When Listeria monocytogenes was infected i.p., gamma delta T cells were induced in the peritoneal cavity of the lck -/- mice. Interestingly, the repertoire of gamma delta T cells was obviously different in the lck +/+ and lck -/- mice; i.e., the gamma delta T cells of the lck -/- mice induced by the listerial infection dominantly expressed V delta 1 while those of the lck +/+ mice dominantly expressed V delta 6. The V delta 1 + gamma delta T cells in the lck -/- mice were extrathymically generated, supported by their appearance in thymectomized irradiated mice reconstituted with bone marrow cells from the lck -/- mice. Furthermore, the gamma delta T cells of the lck +/+ mice were protective in the early stage of the listerial infection, while the gamma delta T cells in the lck -/- mice were not protective against the listerial infection because the depletion of the gamma delta T cells from the lck -/- mice did not influence the bacterial burden in the spleens. These observations thus suggest that 1) gamma delta T cells can develop in adult mice through the intrathymic and extrathymic pathways even in the absence of Lck, 2) Lck influences the expansion and the repertoire of gamma delta T cells, and 3) the gamma delta T cells raised in the absence of Lck are not protective against L. monocytogenes.

Animals↗
PubMedDate not supplied

Metastatic Listeria monocytogenes infection of the peritoneum in mice with cyclosporine a-induced peritonitis.

Inoculation of mice with Listeria monocytogenes intragastrically or by parenteral routes has not been reported to cause peritonitis. In this study, however, severe listerial peritonitis was induced in mice infected subcutaneously and treated intraperitoneally with cyclosporin A (Cs A) in an oil carrier. In both uninfected and listeria-infected mice, intraperitoneal administration of Cs A consistently produced overexpression of P-selectin in the peritoneal microvasculature and pyogranulomatous inflammation of the peritoneum, suggesting that Cs A causes endothelial damage. We suggest that in listeria-infected mice the non-specific irritant peritonitis induced by the intraperitoneal administration of Cs A results in transfer of listeria-infected phagocytes from the liver and spleen to the peritoneal microvasculature, producing metastatic infection.

Animals↗
PubMed1991

Listeriolysin as a virulence factor in Listeria monocytogenes infection of neonatal mice and murine decidual tissue.

Listeriolysin is a 60-kDa protein which allows the growth of Listeria monocytogenes in macrophages and other cells and has been shown to be a virulence factor in Listeria infections of adult mice. However, the neonate and fetoplacental unit are major populations susceptible to listeriosis. Recent data indicate that macrophage and T-cell functions are markedly inhibited in these young mice, and the virulence of listeriolysin-negative (HLY-) and listeriolysin-positive (HLY+) Listeria cells in the setting of such inhibited macrophage and T-cell functions has not previously been examined. We now compare CNL 85/162, a transposon-induced, HLY- Listeria strain, and CNL 85/163, a spontaneous HLY+ revertant. We found that all 18 neonates injected with CNL 85/163 (HLY+) died within 12 days after an injection of 10(4) Listeria cells per mouse. In contrast, all 16 neonates injected with 1,000 times more CNL 85/162 (HLY-) cells survived more than 14 days. Three days after injection, growth of CNL 85/163 (HLY+) in the internal organs was more than 5 log greater than that of CNL 85/162 (HLY-). We also found that CNL 85/162 (HLY-) did not proliferate well in decidual tissue, which is a major component of the placental region. Our studies indicate that HLY- bacteria are not virulent in the neonate and the fetoplacental unit despite the inhibited immune functions at these sites.

Animals↗
PubMed1995

Listeriolysin is processed efficiently into an MHC class I-associated epitope in Listeria monocytogenes-infected cells.

Listeria monocytogenes is an intracellular pathogen that enters the cytoplasm of infected cells by secreting listeriolysin (LLO), a protein that destroys the phagosomal membrane. In infected mice, LLO is a major Ag detected by protective, MHC class I-restricted CTLs. Although the role of LLO in pathogenesis and host immunity is well established, its rate of intracellular synthesis has yet to be determined. Herein we show that cytosolic L. monocytogenes secrete LLO at a relatively low rate of approximately one molecule per bacterium per minute. Under extracellular labeling conditions, the rate of LLO secretion is approximately 50-fold higher. Intracellular LLO synthesis suffices, however, for the accumulation of 600 to 1000 H-2Kd-associated LLO 91-99 epitopes per cell. We calculate that between four and 11 LLO molecules are degraded for each LLO 91-99 epitope bound by H-2Kd. Our findings indicate that the antigenicity of LLO, with respect to MHC class I-restricted CTLs, cannot be attributed to high levels of intracellular secretion. Rather, LLO is a dominant Ag because it is rapidly degraded and very efficiently processed into an MHC class I-associated epitope.

Animals↗
PubMed2000

Pulsed-field gel electrophoresis for the analysis of Listeria monocytogenes infection clusters after kidney transplantation.

Listeria monocytogenes causes a rare, life-threatening infection in recipients of transplanted organs. We used cultures of blood and cerebrospinal fluid to characterize isolates and to distinguish cases in clusters from what might have been sporadic cases. From December 1994 to November 1995, six systemic L. monocytogenes infections occurred at our renal-transplantation unit. We confirmed the clinical diagnosis with blood and cerebrospinal fluid cultures and characterized the isolates retrospectively with pulsed-field gel electrophoresis (PFGE), phage-typing, and serotyping. We also performed an environmental investigation (food, drug, and stool). We took samples after the first two L. monocytogenes infections and then after cases three and four occurred. All patients recovered completely, and no graft was lost. Four patients had identical or genetically related L. monocytogenes isolates in PFGE (type A) and serotyping (type 1/2b). The other two had PFGE type B and G. L. monocytogenes was not detected in food or drug samples from patients on the renal-transplantation ward or in stool samples from the ward staff. It was concluded that PFGE allows sporadic cases and cluster cases of L. monocytogenes infection to be distinguished.

Adult↗
PubMed1985

Effects of cyclosporin A on experimental infection with Listeria monocytogenes.

The effects of cyclosporin A on primary and secondary infection of mice with Listeria monocytogenes was studied both at the microbiological and the histomorphological level. This drug, when given in a dose of 100 mg/kg/day, was found to inhibit the development of protective immunity after primary infection as well as the expression of acquired immunity to challenge infection as determined by counting of bacterial numbers in the spleen. The manifestation of delayed type hypersensitivity was also impaired. When the cellular immune system was functionally intact, the formation of granulomas composed of macrophages and lymphocytes enabled the animals to overcome the Listeria infection. In mice treated with cyclosporin A protective granulomatous reaction during secondary infection did not occur. Instead numerous necropurulent lesions developed in the reticuloendothelial organs, such as spleen and liver, of animals unable to control the lethal infection.

Animals↗
PubMed2006

Invasive Listeria monocytogenes infections in the Netherlands, 1995-2003.

In order to add to the limited data available about the incidence of invasive Listeria monocytogenes infection in the Netherlands, two studies were conducted. In the first study, data on hospital patients with listeriosis in the period 1995-2003 were obtained from the National Medical Registration (study 1). In the second study, hospital discharge letters for patients whose Listeria isolates were received by the Netherlands Reference Laboratory for Bacterial Meningitis (NRLBM) in the period 1999-2003 were retrieved (study 2). Serotyping and pulsed-field gel electrophoresis (PFGE) were used to subtype the various strains of Listeria. These reviews revealed 283 hospital patients and 159 patients with Listeria isolates. Discharge letters were received for 107 (67%) patients. The mean annual incidence of listeriosis in both studies was 2.0 per million inhabitants. The main clinical manifestations were meningitis (incidence: 0.9 and 1.0 per million in studies 1 and 2, respectively) and septicaemia (incidence: 0.08 and 1.0 per million, respectively). Listeriosis in pregnancy was rare (incidence: 1.3 and 2.4 per 100,000 pregnancies over 24 weeks of gestation, respectively). Predisposing conditions were present in 47 and 71% of the patients in studies 1 and 2, respectively. The mortality due to listeriosis was 18%. Serotypes 4b, 1/2a, and 1/2b were responsible for 96% of the cases of human listeriosis. Listeriosis is rare in the Netherlands, but its clinical course is severe and the resulting mortality is high. Therefore, the current recommendations for pregnant women to avoid high-risk foods should be continued. These dietary recommendations should also be given to individuals with predisposing conditions, since they, too, are at risk of Listeria infection.

Adult↗
PubMed1998

Effect of a traditional Chinese medicine, Bu-zhong-yi-qi-tang on the protection against an oral infection with Listeria monocytogenes.

The protective effect against an oral infection with Listeria monocytogenes was observed in BALB/c mice who were orally administered a traditional Chinese medicine, Bu-zhong-yi-qi-tang (Japanese name: Hochu-ekki-to, HOT) daily for 7 days. Bacterial numbers in the Peyer's patch (PP) at 18 h, in the mesenteric lymph nodes (MLN) at 18 h, 1 day and 3 days and in the liver at 3 days after infection were significantly suppressed in HOT-treated mice, although there was no difference in the bacterial number in the small intestinal contents. The enhanced bactericidal activities of PP and liver macrophages by pretreatments of HOT were observed. The protective effect of HOT was not observed in athymic nu/nu and IFN-gamma deficient mice. The administration of HOT increased IFN-gamma-producing cells in the intestinal intraepithelial lymphocytes (IEL) but did not in the PP, MLN and liver. HOT exerts effects mainly on CD8alphabeta+ IEL which are thymus-dependent, and induced IFN-gamma production from their cells. These results suggest that HOT acts on the gut-associated lymphoid tissues and induces IFN-gamma from CD8alphabeta+ IEL, which activates PP and liver macrophages and consequently the resistance to L. monocytogenes is augmented in the mice.

Animals↗
PubMed1992

Role of tumor necrosis factor-alpha and interferon-gamma in newborn host defense against Listeria monocytogenes infection.

The fetus and newborn are particularly susceptible to Listeria monocytogenes infection. We used a newborn rat animal model to investigate neonatal host defense against Listeria. In this animal model, newborn (3-d-old) rats are more susceptible to L. monocytogenes than older animals. Juvenile (23-d-old) L. monocytogenes-infected rats pretreated with lipopolysaccharide (LPS) had a lower bacterial load in blood than control animals, whereas LPS pretreated newborn rats had a higher bacterial load. Because LPS is a potent inducer of tumor necrosis factor (TNF) and TNF enhances host defense against this organism in adult animals, we assessed TNF content in splenic homogenates for animals of different ages. The age at which TNF was detectable in L. monocytogenes-Infected rats corresponded to the age at which LPS became active in preventing severe bacteremia. TNF was less than 1 unit/mL in splenic homogenates taken from rats less than 8 d of age, whereas 16-d-old rats infected with L. monocytogenes 1 d earlier had greater than 80 units/mL (p less than 0.0001 for 3-d-old versus 16-d-old rats). We also assessed the responsiveness of rats to exogenous TNF-alpha. Juvenile rats pretreated with TNF-alpha before L. monocytogenes infection had decreased bacterial load in spleen (p less than 0.02 versus controls) and better survival at 7 d (p less than 0.05 versus controls), whereas newborn rats did not improve with TNF-alpha pretreatment (p greater than 0.05 treated versus controls for splenic bacterial load and 7-d survival).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Systemic and local CC chemokines production in a murine model of Listeria monocytogenes infection.

Repeated intragastric inoculation of Listeria monocytogenes into BALB/c mice resulted in prolonged bacteraemia and severe hepatic infection. Bacteria could also be isolated from the brain tissue of all experimental mice. During the inflammatory process, chemokine concentrations typically increased at the local site in comparison to the systemic level. The liver-to-serum ratio was more pronounced in the case of macrophage inflammatory protein 1 alpha (MIP-1 alpha), suggesting its role in the inflammatory response in the liver. The ratio of brain-to-serum concentration of monocyte chemoattractant protein 1 (MCP-1) remained the same as in the control animals, while it was lower in the infected mice, both in the case MIP-1alpha and in the case of regulated on activation, normal T cell expressed and secreted (RANTES). This is in correlation with slight inflammatory infiltrates found in the brain tissue early in infection.

Animals↗
PubMed1988

The role of hepatic lectins and the activity of the mononuclear phagocyte system in systemic Listeria monocytogenes infection in Balb/c mice.

Hepatic lectin blocking experiments with D-galactose in Balb/c mice showed that parenchymal liver cells are obviously not involved in Listeria monocytogenes infection (strain SLCC 4013, 5 X 10(6) cells i.v.). Using the bacterial immunomodifier Propionibacterium avidum KP-40 the importance of an activated mononuclear phagocyte system in the early stage of Listeria infection could be demonstrated.

Adjuvants, Immunologic↗
PubMed1999

Rat dorsal root ganglia neurons as a model for Listeria monocytogenes infections in culture.

Neurotropism of Listeria monocytogenes was studied in rat dorsal root ganglia (DRG) and hippocampal neurons in culture. Using a system in which the DRG neurons can grow relatively free from other cells, it was observed that such DRG neurons, in contrast to hippocampal neurons, can be effectively infected by L. monocytogenes. The bacteria aligned along DRG axons, but not along hippocampal neurites. A mutant deficient in internalin, a protein required for entry into E-cadherin-expressing cells, did not interact with DRG neurons. Axonal migration of bacteria was studied in the DRG neurons grown in a double-chamber system, where either the neurites or the nerve cell bodies were exposed to the bacteria. The data suggest that L. monocytogenes can infect both axons and DRG nerve cell bodies, and that the bacteria can migrate in a retrograde as well as anterograde direction. These results support the notion that L. monocytogenes can spread via primary sensory neurons to the central nervous system. Infection of DRG primary sensory neurons, as employed in the present study, provides a model for analysis of bacterial and neuronal factors of importance for neurovirulence of L. monocytogenes.

Animals↗
PubMed1984

New perspectives on the gastrointestinal mode of transmission in invasive Listeria monocytogenes infection.

The route or mechanism of transmission of Listeria monocytogenes from its rural veterinary reservoir to newborn and older human populations has been obscure. Anecdotal reports of milk-borne infection from cows with Listeria mastitis have been published, but intensive investigations of small outbreaks of L. monocytogenes infections in humans have not supported a gastrointestinal mode of infection. Several recent studies, however, strongly suggest this possibility, and case-control studies of epidemic listeriosis in the Canadian Maritime provinces in 1981 documented an association between ingestion of uncooked vegetables and the development of illness (p = 0.02). In that study, coleslaw from a regional producer which was distributed throughout the Maritimes was considered to be the vehicle of transmission. Cabbage, the raw product in the production of coleslaw, was contaminated at a farm prior to arrival at the plant. Contamination occurred through fertilization with raw manure from a flock of sheep known to harbour L. monocytogenes. Therefore, an indirect link was established between Listeria monocytogenes infection of sheep on a cabbage farm and subsequent development of invasive listeriosis in humans. This study supports findings from other epidemiologic studies of human listeriosis and is consistent with results of investigations into the mode of transmission of natural and laboratory-acquired listeriosis in animals.

Animals↗
PubMed1987

Passive transfer of acquired resistance to Listeria monocytogenes infection is independent of mononuclear cell granuloma formation.

This study documents the formation of leukocyte foci in the livers of mice infused with either normal or immune T cells and then challenged intravenously with Listeria monocytogenes. The results show that the transfer of antilisterial resistance occurred before mononuclear cell granuloma formation and was associated instead with the appearance of foci of infiltrating lymphocytes and neutrophils. Numbers of these foci remained low in mice which received immune cells but increased progressively until death in mice which received normal cells. These findings do not support the previous hypothesis that a major component of acquired resistance against Listeria infection involves the rapid generation of mononuclear cell granuloma formation under the control of immune T cells.

Animals↗
PubMed1983

Ataxia in Listeria monocytogenes infections of the central nervous system.

From 1976 to 1981 Listeria monocytogenes was second only to Neisseria meningitidis as the cause of bacterial infections of the central nervous system in adults at our hospital. None of the patients with Listeria infection was immunosuppressed or had an underlying malignancy. Ataxia was an initial feature in five of the eight patients, and in three of them it persisted beyond their discharge from the hospital. Ataxia was not a feature of the clinical picture of 14 other adult patients with meningococcal and pneumococcal meningitis. Our data indicate that L monocytogenes should be suspected as the etiologic agent in an adult with ataxia and infection of the central nervous system.

Adult↗