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Listeria monocytogenes, a food-borne intracellular animal and human pathogen, interacts with infected host cells both prior to entry and during the intracellular phase of infection. This review is focused on the role of secreted proteins, including listeriolysin O and two distinct phospholipases C, in modulating the signal transduction of infected cells.
Among the 10 species of the genus Lactobacillus, L. casei showed the strongest protective action against Listeria monocytogenes infection in mice. The activity of L. casei differed with regard to the dose of administration. The anti-L. monocytogenes resistance in mice intravenously administered 5.5 X 10(7), 2.8 X 10(8), or 1.1 X 10(9) L. casei cells was most manifest at ca. 2, 2 and 13, and 3 to 21 days after its administration, respectively. The growth of L. monocytogenes in the liver of mice injected with L. casei (10(7), 10(8), or 10(9) cells) 48 h after infection was suppressed, particularly when 10(8) or 10(9) L. casei cells were given 2 or 13 days before the induced infection, respectively. This suppression of L. monocytogenes growth was overcome by carrageenan treatment or X-ray irradiation. [3H]thymidine incorporation into the liver DNA increased 13 days after administration of L. casei, and augmentation of [3H]thymidine incorporation during 6 to 48 h after infection was dependent on the dose of L. casei. Peritoneal macrophage accumulation observed 1 to 5 days after intraperitoneal injection of UV-killed L. monocytogenes was markedly enhanced when the mice were treated with L. casei cells 13 days before macrophage elicitation. Therefore, the enhanced host resistance by L. casei to L. monocytogenes infection may be mediated by macrophages migrating from the blood stream to the reticuloendothelial system in response to L. casei injection before or after L. monocytogenes infection.
The presence of soluble antigen-antibody complexes renders mice highly susceptible to infection with the intracellular pathogen Listeria monocytogenes. In this report we show that this inhibition is manifest at the level of the innate immune response and is mediated by IL-10. Like immuno-competent mice, mice with the severe combined immunodeficient mutation (SCID) injected with immune complexes died from a sublethal dose of L. monocytogenes. These mice were protected if pretreated with neutralizing antibodies to IL-10. In vitro, immune complexes stimulated IL-10 production by SCID splenocytes and splenic macrophages. Likewise, immune complexes inhibited TNF and IFN-gamma production by SCID splenocytes cultured with heat-killed-L. monocytogenes. This inhibition was reversed by neutralization of IL-10 but not IL-4 or TGF-beta. Immune complexes and rIL-10 inhibited cytokine production by SCID splenocytes if added before or simultaneously with heat-killed-L. monocytogenes. These data support a model in which immune complexes modulate host defense and the immune response by stimulating the production of IL-10 from macrophages.
Listeria monocytogenes has been recognized as a significant pathogen, occurring worldwide, capable of causing animal and human infections. In its most severe form, listeriosis is an invasive disease that affects immunocompromised patients. Additionally, pregnant women represent a high-risk group for L. monocytogenes infection. Abortion, stillbirth or severe neonatal infection can be the serious outcome of such an infection. In an experimental murine model of pregnancy-associated listeriosis we studied the impact of L. monocytogenes on the maternal immune response and pregnancy outcome. In comparison to virgin animals, pregnant mice mounted lower levels of protective cytokines and were unable to eliminate the pathogen. The impaired maternal immune response that has been found both on the systemic and local level, facilitated bacterial multiplication in the liver, placenta and ultimately in the fetal tissues. This resulted in severe necrotizing hemorrhagic hepatitis and Listeria-induced placental necrosis, increasing the incidence of postimplantation loss and poor pregnancy outcome.
Listeria monocytogenes is highly susceptible to meropenem in vitro, but data on the efficacy of meropenem in clinical cases of listeriosis are scarce. Described here is the case of a child with aplastic anemia who acquired nosocomial listeriosis and failed to respond to initial meropenem therapy. Resolution of fever was not noted after 5 days of therapy with meropenem and, more importantly, clinical worsening was observed during this period. The patient began to improve after ampicillin was introduced to the therapeutic regimen. In total, meropenem was administered for 15 days and ampicillin for 10 days.
Listeria monocytogenes is a gram-positive bacillus that causes meningitis, encephalitis, bacteremia, and febrile gastroenteritis. Most disease occurs in immunosuppressed individuals. Recent seroepidemiologic studies show that the infection is foodborne. Due to the increasing number of immunosuppressed individuals at risk for listeriosis, as well as the persistence of substantial foodborne outbreaks, L. monocytogenes has gained worldwide attention as an important pathogen. Heightened surveillance and quality control by the food industry have been instituted, leading to a reduction in the number of cases and deaths from this infection in the past decade. However, due to the ubiquity of the organism in the environment, outbreaks and sporadic disease continue to occur. The standard therapy for listeriosis is a combination of ampicillin and gentamicin or, for patients who are intolerant of b-lactam agents, trimethoprim-sulfamethazole. Despite the availability of therapy, the mortality rate remains high in those with T-cell immunodeficiencies.
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Listeriolysin O (LLO) is a secreted pore-forming toxin of the facultative intracellular bacterium Listeria monocytogenes. We assessed the ability of a murine anti-LLO mAb to affect the course of infection in mice challenged with Listeria. This mAb was previously shown to be capable of neutralizing LLO-mediated pore formation in vitro, and here we show that the passive administration of this Ab to mice before infection provides increased resistance. Mice treated with the mAb were protected from a lethal challenge with virulent Listeria and showed a significant reduction in Listeria burden during the first hours to days postinfection. These effects of the Ab were independent of host B or T cells, since treatment with the mAb provided enhanced resistance to SCID mice. The titer of anti-LLO Abs during the regular infection of mice with Listeria was found to be low to negative.
A system of primers for detection of Listeria by polymerase chain reaction (PCR) has been developed. Specificity and sensitivity of the method was evaluated by analyses of reference clinical and abiotic samples. Clinical trials of PCR were carried by detecting latent (asymptomatic) carriers of Listeria among healthy women of epidemiologically significant professions. PCR is characterized by numerous advantages in comparison with the traditional bacteriological analysis.
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Aged mice of the CBA/Ca strain, 15 months of age, and A/J mice, 17 months of age, exhibited impaired lymphoblastogenic response to concanavalin A but not to lipopolysaccharide. This defective cellular responsiveness was not accompanied by decreased antibody response to protein antigen or decreased ability to develop delayed hypersensitivity to picryl chloride. An increased susceptibility to influenza virus infection given intranasally was noted in the aged mice as compared with young animals. Such virus infection also impaired the lymphoblastogenic response to mitogens. Surprisingly, the virus infection in aged animals was less lethal after a subsequent infection with a small inoculum of Listeria bacteria.
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Cell wall, cytoplasm, polysaccharide, and peptidoglycan fractions prepared from Lactobacillus casei, L. plantarum, and L. acidophilus were examined for their efficacies to enhance resistance of host mice against Listeria monocytogenes infection. Intraperitoneal injections of those cellular fractions of L. casei led to elicitation of inflammatory cells in the peritoneal cavity and the efficacy was highest in the case of peptidoglycan. Macrophage ratio in the resultant peritoneal exudate cells was also highest in mice given peptidoglycan. Macrophages induced with cell wall fraction of L. casei showed the most potent phorbol myristate acetate (PMA)-triggered respiratory burst (chemiluminescence and O2- production determined on the basis of nitroblue tetrazolium reduction) followed by those elicited with peptidoglycan. All the macrophages induced with cell wall of L. casei (two strains) and L. acidophilus enhanced O2- production in response to PMA but L. plantarum did not enhance O2(-)-producing ability in such a manner. The L. casei-cell wall also enhanced in vitro listericidal activity of mouse peritoneal macrophages, but such an activity was not noted in the case of L. acidophilus-cell wall. When mice were intravenously given the cellular fractions 7 or 13 days before L. monocytogenes infection, cell wall fractions of L. casei caused the most potent protective activity. A weak protective activity was also found in peptidoglycan of L. casei. Therefore, the protective action of L. casei against L. monocytogenes infection in host mice may be attributed to cell wall compounds and partially to the peptidoglycan moiety.
Listeria species are Gram-positive bacilli, present in food and in the environment (soil, water). Most of them are fortunately low-virulent, so there is no risk for healthy people. However, in special circumstances, they can be pathogenic, in immunocompromised individuals. Septicaemia in pregnancy is not dangerous for women, but for the foetus, so delayed diagnosis will lead to spontaneous abortion, intrauterine death or eventually to premature labour. We report in our paper case of Listeria septicaemia in a pregnant woman in the third trimester of the pregnancy. Thanks to early diagnosis and subsequent causal antibiotic treatment, we were able to prevent the development of congenital infection and a healthy baby was born.