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PubMed1998

Mice lacking the murine interleukin-8 receptor homologue demonstrate paradoxical responses to acute and chronic experimental infection with Listeria monocytogenes.

In this study we demonstrate that mice which lack the murine interleukin-8 receptor homologue exhibit enhanced resistance during the early stage of infection (1-4 days after i.v. challenge with Listeria monocytogenes). This result is surprising in that interleukin-8 and other CXC chemokines are key players in the accumulation of inflammatory neutrophils, which is thought to be critical for resistance to listeriosis. Paradoxically, some of the interleukin-8 receptor knockout mice that survived acute infection with L. monocytogenes demonstrated evidence of chronic infection with L. monocytogenes.

Acute Disease↗
PubMed1999

The effects of Chlorella vulgaris in the protection of mice infected with Listeria monocytogenes. Role of natural killer cells.

In this work we have demonstrated the effects of oral administration of Chlorella vulgaris (CV) on Natural Killer cells (NK) activity of mice infected with a sublethal dose of viable Listeria monocytogenes. The treatment with C. vulgaris produced a significant increase on NK cells activity in normal (non-infected) animals compared to the animals that received only vehicle (water) (p < 0.0001). Similarly, the infection alone produced a significant increase on NK cells activity, which was observed at 48 and 72 hours after the inoculation of L. monocytogenes. Moreover, when CV was administered in infected animals, there was an additional increase in NK cells activity which was significantly higher than that found in the infected groups (p < 0.0001). CV treatment (50 and 500mg/Kg) of mice infected with a dose of 3 x 10(5) bacteria/animal, which was lethal for all the non-treated controls, produced a dose-response protection which led to a 20% and 55% survival, respectively (p < 0.0001).

Animals↗
PubMedDate not supplied

Stimulation of cell-mediated resistance in mice to infection with Listeria monocytogenes by vitamin A.

Vitamin A given as retinol-acetate, retinol-palmitate as well as the derivates retinoic acid and a retinoid, strongly fortified the resistance of mice to infection with virulent cells of Listeria monocytogenes. However, strong enhancement of resistance was only achieved when high toxic doses of vitamin A were given. Apparently, this effect was due to a stimulation of the function of the mononuclear phagocytic system rather than of the T lymphocyte.

Animals↗
PubMed1996

The pathogenesis of infection by Listeria monocytogenes.

Listeria monocytogenes is a Gram-positive bacterium responsible for severe infections in human and a large variety of animal species. It is a facultative intracellular pathogen which invades macrophages and most tissue cells of infected hosts where it can proliferate. The molecular basis of this intracellular parasitism has been to a large extent elucidated. The virulence factors, including internalin, listeriolysin O, phospholipases and a bacterial surface protein, ActA, are encoded by chromosomal genes organised in operons. Following internalisation into host cells, the bacteria escape from the phagosomal compartment and enter the cytoplasm. They then spread from cell to cell by a process involving actin polymerisation. In infected hosts, the bacteria cross the intestinal wall at Peyer's patches to invade the mesenteric lymph nodes and the blood. The main target organ is the liver, where the bacteria multiply inside hepatocytes. Early recruitment of polymorphonuclear cells lead to hepatocyte lysis, and thereby bacterial release. This causes prolonged septicaemia, particularly in immunocompromised hosts, thus exposing the placenta and brain to infection. The prognosis of listeriosis depends on the severity of meningoencephalitis, due to the elective location of foci of infection in the brain stem (rhombencephalitis). Despite bactericidal antibiotic therapy, the overall mortality is still high (25 to 30%).

Actins↗
PubMed1990

Suppression of host resistance against Listeria monocytogenes infection by 15-deoxyspergualin in mice.

The effects of 15-deoxyspergualin (DSG), an immunosuppressive agent, on host resistance against Listeria monocytogenes were studied in mice. Administration of DSG in the early phase of infection resulted in fatal listeriosis by preventing acquired anti-listerial resistance, even though the infectious dose was sublethal for the untreated controls. In contrast, DSG treatment started after development of the acquired immunity was ineffective. Endogenous production of interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) in the bloodstreams induced by the infection was normal in DSG-treated mice. Nevertheless, augmentation of macrophage functions such as expression of major histocompatibility complex (MHC) class II antigens, phagocytic activity and listericidal activity induced by the infection was abrogated by DSG treatment. These results suggest that the inhibitory effect of DSG on anti-listerial resistance might be different from cyclosporine A (CsA).

Animals↗
PubMed1987

Inhibition of macrophage-mediated antigen presentation by hemolysin-producing Listeria monocytogenes.

T lymphocytes and macrophages from Listeria-infected mice were used to evaluate the processing and presentation of live Listeria monocytogenes in vitro. Antigen presentation to T cells was quantitated by interleukin-2 production. In contrast to inert antigens such as heat-killed Listeria, live bacteria were processed and presented poorly. To evaluate the role of hemolysin (Hly), we used isogenic pairs of Hly+ and Hly- Listeria as antigens. In contrast to live Hly- bacteria, which were presented as well as heat-killed Listeria, live Hly+ bacteria were presented poorly. Hly+ bacteria also inhibited the presentation of heat-killed Listeria. This effect was apparent with as few as 10 bacteria/macrophage and was not due to loss of macrophage viability or decreased Ia expression after exposure to the live bacteria. With respect to murine listeriosis, the LD50 values for the Hly- strains were at least 1000 times higher than those for the Hly+ strains. These results suggest that the ability of Hly+ bacteria to inhibit antigen processing and presentation may be an important determining factor in Listeria infection and immunity.

Animals↗
PubMed2004

Lack of apoptosis in Listeria monocytogenes-infected thymocytes from mice fed with dietary lipids.

The potential action of certain fatty acids has been studied since the early 1970s. Numerous effects on immune system functions have been related to dietary lipid administration; therefore, several of them have been applied in the treatment of inflammatory disorders. Nevertheless, n-3 polyunsaturated fatty acids may affect host resistance to infectious diseases. In addition, several studies have demonstrated that certain fatty acids are involved in apoptosis induction. Here, we have examined the action of different dietary lipids on the promotion of apoptosis in thymocytes from mice fed with dietary lipids and infected with Listeria monocytogenes. Thus, L. monocytogenes promoted an important cytotoxic effect in all of the groups, but it did not increase the percentage of DNA fragmentation. Similarly, an important increase of caspase-3 activity was demonstrated in OO and FO groups, but infection with L. monocytogenes exerted an inhibitory effect. Finally, L. monocytogenes did not modify proteasome activity among groups fed with dietary lipids. On the basis of this preliminary study, we can state that the infection of thymocytes from mice fed with dietary lipids does not promote a synergistic effect in the induction of apoptosis. Hence, these results may partially serve to elucidate the immune mechanisms involved in cells from mice fed with dietary lipids in an infectious process.

Animals↗
PubMed2000

Human dendritic cells infected by Listeria monocytogenes: induction of maturation, requirements for phagolysosomal escape and antigen presentation capacity.

An important feature of microbial infections is the ability of the microorganisms to interfere with and modulate the induction of host immune reactions. However, little is known about the effects of broad host range pathogens such as Listeria monocytogenes on similar cell types in different hosts. Here we examine the effects of the human and animal pathogen L. monocytogenes on human dendritic cells (DC) since this type of cells is essential for the initiation of immune responses. Listeria are phagocytosed efficiently by immature human DC and the bacteria escape from the phagolysosome quickly. Lack of the pore-forming activity of listeriolysin, which was found to be essential for the vacuolar escape of this bacterium in other cell types, retarded but did not prevent egress from the vacuole. Treatment of cultures of immature DC with L. monocytogenes resulted in rapid changes in morphology and cellular constitution followed by maturation of the DC. This could be judged by the appearance of maturation-specific cell surface markers. Antigen presentation to CD4 T cells was apparently not impaired by the infection. These results are in clear contrast to results obtained previously in the mouse system (Guzman et al., Mol. Microbiol. 1996. 20: 119 - 126; Darji et al., Eur. J. Immunol. 1997. 27: 1696 - 1703.).

Antigen Presentation↗
PubMed1995

Listeria monocytogenes infection in pregnant mice: abnormalities in the function of non-adherent accessory light density dendritic cells.

Pregnant A/J mice were found to be more susceptible to the lethal effect of Listeria monocytogenes bacteria than virgin females. However, during the first four days of post-infection there was no difference in the elimination of Listeria from the spleens of pregnant and virgin mice. This suggests that the increase in the susceptibility of pregnant mice to pathogenic activity of L. monocytogenes was related to the diminution in Listeria-specific cellular reactions. Indeed, we found that non-adherent light density dendritic cells (DCs) from pregnant mice showed a marked reduction in the ability to form clusters with L. monocytogenes immune T lymphocytes and it is known that cell cluster formation between antigen presenting cells (APC) and responding T cells is required for antigen recognition as well as for cell proliferation. DCs from pregnant mice also demonstrated the decrease and an instability in the expression of H-2 class II molecules which play a crucial role in the recognition of exogenous antigens. The abnormalities demonstrated in the function of the light density dendritic cells from the spleens of pregnant mice could compromise cellular reactions to L. monocytogenes bacteria possibly resulting in increased susceptibility of pregnant mice to experimental listeriosis.

Animals↗
PubMedDate not supplied

[Listeria monocytogenes nosocomial infection in the maternity ward].

Nosocomial infection with Listeria monocytogenes 4b occurred in January 1990 in a maternity hospital in Grenoble. The 3 patients involved were born within a 24 hour-interval. The premature newborn responsible for contamination was asymptomatic. Two other newborns without any perinatal infectious risk presented with meningitis, one on the 5th day of life in the maternity hospital, the other one on the 11th day while already at home. The 3 strains of Listeria had the same serovar and lysovar. Epidemiologic investigations led to suspect a contamination in the delivery room and during the care of the children. Strict respect of hygiene orders is imperative to avoid nosocomial infections.

Cross Infection↗
PubMed1983

Chemical composition and biological functions of Listeria monocytogenes cell wall preparations.

A crude Listeria cell wall fraction, a purified fraction (PF) with demonstrated biological activity, as well as a third fraction of base-hydrolyzed PF (BHPF) were analyzed for chemical composition and activities not previously described. Listeria cell wall fraction and PF contained significant quantities of lipid, whereas BHPF was lipid depleted. Fatty acid compositions were typical of gram-positive bacteria. PF and BHPF were depleted in protein. Alanine, glutamic acid, diaminopimelic acid, glucosamine, and muramic acid were found in all fractions, in enhanced concentration in PF and BHPF, and with molar ratios typical of bacterial peptidoglycans. Major neutral sugars were rhamnose, ribose, ribitol, and glucose. The concentrations of rhamnose, ribose, and glucose were increased in BHPF. Differences in chemical composition of the fractions reflected differences in their biological activities: Listeria cell wall fraction induced resistance to Listeria infection, whereas PF did not. Mitogenic and adjuvant activities were demonstrated for Listeria cell wall fraction and PF but were lost in BHPF. BHPF retained the ability to induce macrophage-mediated tumoricidal activity and decrease resistance to Listeria infection.

Adjuvants, Immunologic↗
PubMed2006

Prophylactic administration of Withania somnifera extract increases host resistance in Listeria monocytogenes infected mice.

In this study, we demonstrated that Withania somnifera L. extract (WSE) protects mice from a lethal dose of Listeria monocytogenes when administered prophylactically at 100, 250 and 500 mg/kg for 10 days, with survival rates up to 30%. These doses also prevented the myelosuppression and the splenomegaly caused by a sublethal infection with L. monocytogenes, due to increased numbers of granulocyte-macrophage progenitors (CFU-GM) in the bone marrow. Investigation of the production of colony-stimulating factors (CSFs) revealed increased colony-stimulating activity (CSA) in the serum of normal and infected mice pre-treated with WSE. Further studies to investigate the levels of interferon-gamma (INF-gamma) and lymphocyte cell proliferation were undertaken. We observed dose-dependent increases in cell proliferation and in the levels of INF-gamma in mice infected with L. monocytogenes and treated with WSE. All together, our results suggest that WSE indirectly modulates immune activity and probably disengages Listeria-induced suppression of these responses by inducing a higher reserve of myeloid progenitors in the bone marrow, proliferation of lymphocytes and increased INF-gamma levels.

Animals↗
PubMed2001

Exaggerated proinflammatory and Th1 responses in the absence of gamma/delta T cells after infection with Listeria monocytogenes.

While gamma/delta T cells are involved in host defense and immunopathology in a variety of infectious diseases, their precise role is not yet clearly defined. In the absence of gamma/delta T cells, mice die after infection with a dose of Listeria monocytogenes that is not lethal in immunologically intact animals. Morbidity might result from insufficient levels of cytokines normally produced by gamma/delta T cells or conversely from an excess of cytokines due to a lack of down-regulation of the inflammatory response in the absence of gamma/delta T cells. Consistent with a regulatory role, we found that systemic levels of proinflammatory cytokines (interleukin-6 [IL-6], IL-12, and gamma interferon [IFN-gamma]) were significantly higher in the absence of gamma/delta T cells during the innate phase of the response. Using combinations of genetically altered and immunodepleted mice, we found evidence for gamma/delta T-cell-mediated regulation of IFN-gamma production by multiple cell types of both lymphoid and myeloid lineages. The antigen-specific alpha/beta T-cell response that followed the exaggerated innate response was also increased in gamma/delta T-cell-deficient mice. These findings are consistent with an emerging picture from a variety of immune response models of a critical role for gamma/delta T cells in down-modulation of the immune response.

Adaptation, Biological↗
PubMed1978

Acquired cellular resistance, delayed hypersensitivity, and altered macrophage migration in Listeria monocytogenes-infected guinea pigs.

A Listeria monocytogenes infection in guinea pigs was used to study the interrelationship between antigen-induced macrophage migration inhibition, delayed-type hypersensitivity, and acquired cellular resistance. Early after infection (at 2 and 7 days), very significant enhancement of macrophage migration was observed. Migration inhibition was detected beginning on day 14 and was uniformly observed only on day 21 of the infection, after which a shift again to enhancement was seen. The early detection (by day 2) of migration enhancement suggested that this assay may be more sensitive than assessment of delayed type hypersensitivity in vivo, which in this system was first detectable only on day 4. Acquired cellular resistance, as measured by enhanced survival following a high dose challenge with Listeria, was present from day 7 after infection until at least day 60. By splenic clearance studies, however, acquired cellular resistance was present only until day 14 after infection, suggesting that in this system splenic clearance was not a very reliable criterion for measuring acquired cellular resistance.

Animals↗
PubMed1999

Effects of Chlorella vulgaris on bone marrow progenitor cells of mice infected with Listeria monocytogenes.

In this study we investigated the effects of the treatment with Chlorella vulgaris extract (CVE) on the hematopoietic response of granulocyte-macrophage colony-forming unit (CFU-GM) of mice infected with a sublethal dose of Listeria monocytogenes (1 x 10(4) organisms/animal). CVE was given orally as 50 mg/kg/day for 5 days. In the CVE treated/infected groups L. monocytogenes was administered at the end of CVE treatment. The colony stimulating activity of the serum (CSA) was also studied in all groups. Although no effects on CFU-GM, as compared to controls, were observed in the groups receiving CVE alone, the extract produced an increase in CSA levels as compared to controls. On the other hand, the presence of the infection led to a significant reduction in the numbers of CFU-GM as observed at 48 and 72 h after the infection, in spite of the significant increase in serum CSA activity. CVE treatment of infected animals restored the numbers of CFU-GM to control levels. In the treated/ infected group the increased serum CSA was significantly higher than that observed in the only infected group. The CVE treatment (50 and 500 mg/kg) of mice infected with a dose of 3 x 10(5) bacteria/animal, which was lethal for all the non-treated controls, produced a dose-response protection which led to a 20 and 52% survival, respectively. These results demonstrated that CVE produces a significant increase in the resistance of the animals infected with L. monocytogenes, and that this protection is due, at least in part, to increased CFU-GM in the bone marrow of infected animals.

Administration, Oral↗
PubMed2002

[Food-borne infections: do we need further data collection for public health action and research].

The data needed for controlling and preventing food-borne infectious diseases relied so far on surveillance of the main food-borne infections (Salmonella and listeria infections) to follow trends over time and detect outbreak. However, this systematic continuous data collection was not always sensitive enough to timely detect community outbreaks and did not take into account sporadic cases of food-borne infections which represent the majority of patients (such as Campylobacter infection for example). Therefore, the true burden of food-borne infections, including morbidity, mortality and the social and economic cost could not be assessed. As the issue of food-borne infections got more social attention, the need of further epidemiological data has increased including the implementation of large population studies (active surveillance and follow up studies) associated with analytical studies in the United States (Foodnet) and in some European countries (United Kingdom, The Netherlands, Denmark.). Meanwhile surveillance and detection of outbreaks have substantially improved through the use of new typing scheme, particularly those based on molecular techniques. Their routine use, now, allows an early identification of the clonal spread of food-borne bacteria. The application of automatic detection algorithm to surveillance data base has also improved the performance of outbreak detection and changes of trends. Furthermore, food-borne infection surveillance has become European which allows, by pooling of national database, to identify emergence that did not get noticed in any country. To foster the prevention of sporadic cases, the use of analytical epidemiology has become more and more frequent and has improved the knowledge of food vehicles and risk factors. The risk assessment approach has also been applied to the microbial contamination of food to answer to the increasing needs of expertise, particularly at the international level. This approach, however, needs further methodological development and the collection of extra information on the food chain. Last, but not the least, a wider public health research approach must also be considered, particularly on the social perception of food-borne risks and the cost-effectiveness analysis of the prevention measures that are taken.

Adult↗