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PubMedDate not supplied

[A case of maternal and neonatal infection due to Listeria monocytogenes].

A Listeria monocytogenes infection may develop during pregnancy by eating sausages, fresh meats and milk products derived from infected animals. According to the period in which the infection starts, the pregnancy outcome can be abortion or pre-term or at term delivery. The infection can pass from mother to fetus and can cause a serious neonatal sepsis. Listeriosis in pregnant women can be asymptomatic or may present as an influenza-like syndrome. This case report, along with other published cases, demonstrates how hard is to make a correct diagnosis of listeriosis during pregnancy. Since this is mainly related to the aspecificity of symptoms, it is very important to have a high suspicion and to take a careful patient history.

Acetaminophen↗
PubMed1995

Listeria monocytogenes infection increases neutrophil adhesion and damage to a murine hepatocyte cell line in vitro.

Several studies have reported that Listeria monocytogenes multiples within hepatocytes and that inflammatory neutrophils inhibit this intracellular growth in vivo. In the present study, we used a murine embryonic hepatocyte cell line (ATCC TIB73) as an in vitro model to investigate neutrophil-hepatocyte interactions. Murine peritoneal exudate neutrophils adhered more readily to L. monocytogenes-infected hepatocyte monolayers than to uninfected monolayers or monolayers infected with actA- and hly- mutants of L. monocytogenes. L. monocytogenes-infected TIB73 cells increased their surface expression of ICAM-1 as compared with uninfected TIB73 cells. Neutrophil adherence and oxidative stress to TIB73 cells were reduced by pre-incubating the hepatocyte monolayers with anti-ICAM-1 monoclonal antibody and diminished further by pre-incubating the peritoneal exudate neutrophils with an anti-CR3 monoclonal antibody.

Animals↗
PubMed2004

Lactoferricin influences early events of Listeria monocytogenes infection in THP-1 human macrophages.

Bovine lactoferrin (BLf) and its derivative peptide lactoferricin B (LfcinB) are known for their antimicrobial activity towards several pathogens, including Listeria monocytogenes, a food-borne Gram-positive invasive bacterium that infects a wide variety of host cells, including professional phagocytes. To add further information on the antibacterial effects of these compounds, the influence of BLf, LfcinB and the antimicrobial centre of LfcinB, the hexapeptide LfcinB(4-9), on the invasive behaviour of L. monocytogenes was analysed in IFN-gamma-activated human macrophagic cells (THP-1). Significant inhibition of bacterial entry in THP-1 cells was observed at LfcinB concentrations that were unable to produce any bacteriostatic or bactericidal effect, compared with BLf and LfcinB(4-9) peptide. This inhibition occurred when LfcinB was incubated during the bacterial infection step and was not due only to competition for common glycosaminoglycan receptors. Assays performed through a temperature shift from 4 to 37 degrees C showed that inhibition of invasion took place at an early post-adsorption step, although an effect on a different step of intracellular infection could not be ruled out.

Animals↗
PubMedDate not supplied

[Analysis of the immune resistance in an experimental murine model fed dietary lipids and infected with Listeria monocytogenes].

Several dietary lipids are capable of exerting an immunosupressor effect. This action may have undiserable effects on the host immune resistance to infectious diseases. The purpose of the present study was to determinate the immune status of mice fed dietary lipids and experimentally infected with a virulent strain of Listeria monocytogenes. Balb/c mice were divided into four groups and were fed with their respective diet: low fat diet (LF, 20%), olive oil diet (OO, 20%), fish oil diet (FO, 20%) and hydrogenated coconut oil (HCO, 20%). Mice were fed for four weeks and infected with L. monocytogenes by endovenous route. Results have shown a survival reduction in mice fed a diet containing FO, as well as a significant increase in the number of viable bacteria from spleen. In addition, we have observed an increase in the bactericidal activity in peritoneal cells from OO group, although the invasion of L. monocytogenes in cells from this group was larger. Finally, a significant reduction of lymphocyte proliferation was observed in the group fed an FO diet, whereas natural killer (NK) cell activity was not modified. These results indicate that dietary lipids constituted by polyunsaturated n-3 fatty acids reduce the murine immune resistance, whereas a diet constituted by OO-does not exert an immunosuppressor effect as relevant as FO diet, and it does not reduce the immune resistance leading to an efficient L. monocytogenes elimination.

Animals↗
PubMed1995

Listeria monocytogenes infects human endothelial cells by two distinct mechanisms.

Infection of endothelial cells by bacteria may be an important component of the bacteria's ability to escape host defenses and cause disease. Listeria monocytogenes cause sepsis and central nervous system infection in domesticated animals and immunocompromised humans, suggesting that this bacterium interacts with endothelial cells in a significant fashion. The experiments presented here tested the hypothesis that L. monocytogenes can invade and replicate within human endothelial cells. We found that L. monocytogenes grows readily in umbilical vein endothelial cells and that its intracellular life cycle involves phagosomal escape, F-actin-based motility, and cell-to-cell spread. We found that L. monocytogenes invaded endothelial cells by cell-to-cell spread from adherent mononuclear phagocytes which were previously infected by this bacterium. Interestingly, L. monocytogenes mutants lacking the invasion protein, internalin, bound less well to endothelial cells than did wild-type bacteria in the absence, but not the presence, of serum, and their invasion of endothelial cells was diminished under both conditions. Thus, endothelial cell infection by L. monocytogenes can occur by two distinct mechanisms: direct bacterial invasion of the endothelial cells in an internalin-mediated fashion or cell-to-cell spread from adherent, infected mononuclear phagocytes. These data support the idea that endothelial cell infection by L. monocytogenes is an important event in the pathogenesis of listeriosis.

Actins↗
PubMed1994

Antigen-specific T-cell responses during primary and secondary Listeria monocytogenes infection.

Although murine listeriosis is a widely used experimental model for the analysis of cell-mediated immunity, there is little information about individual T-cell antigens of Listeria monocytogenes which are recognized during primary and secondary infection. To study the antigen responses of L. monocytogenes-reactive T cells, somatic and secreted listerial proteins were separated by two-dimensional gel electrophoresis and subsequently divided into 480 liquid fractions. Antigen-specific T cells isolated from mice at different times of primary and secondary listeriosis were tested for their capacity to proliferate with distinct protein fractions. Supernatants of these cultures were screened for the production of gamma interferon, interleukin-4 (IL-4), and IL-10. Proliferation of antigen-specific T cells correlated with the production of high concentrations of gamma interferon, whereas IL-4 and IL-10 production in response to listerial protein fractions could not be detected. During both primary and secondary listeriosis, T cells recognized a multitude of somatic and secreted proteins rather than one or a few dominant antigens. Secreted proteins were recognized before somatic proteins, and T cells recognized different fractions in secreted and somatic proteins.

Animals↗
PubMed2003

Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). II. Effects of DEPs on T-cell-mediated immune responses in rats.

Previously, we showed that diesel exhaust particles (DEPs) suppressed pulmonary clearance of Listeria monocytogenes (Listeria) and inhibited the phagocytosis of alveolar macrophages and their response to Listeria in the secretion of interleukin (IL)-1 beta, tumor necrosis factor alpha, and IL-12. In this report we examined the effects of DEPs and/or Listeria on T-cell development and secretion of IL-2, IL-6, and interferon (IFN)-gamma. We exposed Brown Norway rats to clean air or DEPs at 50 or 100 mg/m3 for 4 hr by nose-only inhalation and inoculated with 100,000 Listeria. Lymphocytes in the lung-draining lymph nodes were isolated at 3 and 7 days postexposure, analyzed for CD4+ and CD8+ cells, and measured for cytokine production in response to concanavalin A or heat-killed L. monocytogenes. Listeria infection induced lymphocyte production of IL-6. At 7 days postinfection, lymphocytes from Listeria-infected rats showed significant increases in CD4+ and CD8+ cell counts and the CD8+/CD4+ ratio and exhibited increased production of IFN-gamma and IL-2 receptor expression compared with the noninfected control. These results suggest an immune response that involves the action of IL-6 on T-cell activation, yielding Listeria-specific CD8+ cells. DEP exposure alone enhanced lymphocyte production of both IL-2 and IL-6 but inhibited lymphocyte secretion of IFN-gamma. In rats exposed to 100 mg/m3 DEPs and Listeria, a 10-fold increase occurred in pulmonary bacterial count at 3 days postinfection when compared with the Listeria-only exposure group. The isolated lymphocytes showed a significant increase in the CD4+ and CD8+ cell counts and the CD8+/CD4+ ratio and exhibited increased IL-2 responsiveness and increased capacity in the secretion of IL-2, IL-6, and IFN-gamma. This T-cell immune response was sufficient to allow the Brown Norway rats to clear the bacteria at 7 days postinfection and overcome the down-regulation of the innate immunity by the acute DEP exposure.

Air Pollutants↗
PubMed1984

Protective mechanisms against infection by Listeria monocytogenes: accumulation and activation of macrophages.

The protective mechanisms against Listeria monocytogenes were analysed in mice. Listeria immune mice were rechallenged with viable listeria, and the degree of activation of macrophages, the degree of accumulation of macrophages to the infected sites, and these mechanisms were studied. Enhanced acquired resistance to the reinfection became detectable from the early stage of immunization. It was observed that activation of macrophages was mediated by pretreatment with antigen from the early stage of immunization. Enhanced accumulation of macrophages at the infected sites was observed only in the early stage. Enhanced accumulation and activation of macrophages in the early stage were generated by mediators from listeria antigen sensitized T lymphocytes which were different from classical tuberculin type. Enhanced activation of macrophages in the later stage was generated by MAF and/or MIF from sensitized T lymphocytes of classical tuberculin type. It was suggested that acquired cellular resistance to listeria in the early stage depends on both activation and accumulation of macrophages, and that in the later stage depends on activation of macrophages.

Animals↗
PubMed1975

The mediator of cellular immunity. IX. The relationship between cellular hypersensitivity and acquired cellular resistance in rats infected with Listeria monocytogenes.

Acquired resistance to the intracellular bacterial parasite, Listeria monocytogenes can be transferred to normal recipients by thoracic duct lymphocytes or peritoneal exudate cells obtained from rats infected with this organism; The appearance of protective cells in thoracic duct lymph coincides with the development in the donors of delayed-type hypersensitivity to Listeria antigens and accumulation in induced peritoneal exudates of cells which are responsive to these antigens in the migration inhibitory factor (MIF) assay. The cells in exudates that confer protection, and those that release MIF, arise at sites remote from their final destination. From their point of origin in the caudal lymph nodes of infected rats, cells with these properties are delivered to the thoracic duct and hence to the blood from where they are drawn into the peritoneal cavity in response to inflammation. The parallel observed in the appearance, increase and subsequent decline of protective lymphocytes and MIF-producing cells in exudates suggest that the two activities are mediated by a single line of T cells. However this may be, the development and deployment of the cells concerned encourages the belief that MIF has a meaningful role in the expression of cellular resistance to infection.

Animals↗