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PubMed2004

The role of CD1d in the immune response against Listeria infection.

To address the role of CD1d in mucosal immune regulation in bacterial infection, we infected CD1d KO mice with Listeria monocytogenes (Lm). A higher systemic bacterial burden associated with inflammatory lymphocytic infiltrations within the intestine was found in CD1d KO compared with wild type (WT) mice. Lm induced strong IFN-gamma mRNA expression in the liver of WT and the intestine of CD1d KO mice, thus demonstrating the dual, opposing immune activities of IFN-gamma in Lm infection that is dependent on CD1d and/or NKT cells. Analysis of hepatic T cell population demonstrated a reduction of NK1.1(+)TCRbeta+ cells in both mice, followed by recovery only in WT mice. Last, the proportion of alpha4beta1 integrin on lung lymphocytes from CD1d KO was dramatically increased compared with WT mice. Thus, the absence of CD1d resulted in increased susceptibility towards Listeria infection, induced changes in NKT cells, and increased trafficking of alpha4beta1 molecule to inflamed lung.

Animals↗
PubMed1997

Lymphocyte apoptosis during early phase of Listeria infection in mice.

During the acute phase of growth of Listeria monocytogenes in spleen and lymph nodes, the infective foci consist of macrophages and neutrophils accompanied by extensive death of lymphocytes. Many of the lymphocytes die by apoptosis. The lesions are found by 48 hours after infection and can regress with time. Depending on the dose, the infected foci can be restricted to the thymus-dependent areas or can occupy the entire lymphoid tissue. The Listeria in the lesions are primarily found inside macrophages, but a few are extracellular amid cellular debris. Lymphocyte death appears to be an obligatory step in primary Listeria infection, the extent of which is controlled by the early restriction of Listeria growth by the innate cellular system.

Animals↗
PubMed2002

Listeria infection during pregnancy: a 10 year experience.

BACKGROUND: Although Listeria monocytogenes is widely distributed in nature, it rarely causes clinical infection in previously healthy people. This microorganism, however, may cause severe invasive disease in pregnant women and newborns. OBJECTIVES: To investigate--in our pregnant population--the impact, severity and outcome of listeriosis on both mother and fetus. METHOD: The study was carried out at a level III, university two-hospital complex. In a retrospective chart review of 65,022 parturients during a 10 year period (1990-1999), we identified and evaluated 11 pregnant patients and their offspring with Listeria infection. RESULTS: Chorioamnionitis with multiple placental abscesses were observed in all five placentae examined. Clinically, 4 of 11 parturients had a cesarean section for fetal distress (36.3%), as compared to the 14% mean CS rate in our general population. Two of 11 had a late abortion (18.1%), as compared with the 4% rate in our hospital. Four of 11 had premature labor (36%), which was about four times the rate in our population. Finally, although no intrauterine fetal death was recorded in our series, there was one neonatal death of a term infant (1/11, 9%), which is about 10 times higher than our corrected perinatal mortality rate. CONCLUSIONS: If not promptly and adequately treated, listeriosis in pregnancy may present serious hazards to the fetus and newborn through direct infection of the placenta and chorioamnionitis.

Adult↗
PubMed1993

The cellular source of interleukin-6 during Listeria infection.

The cellular source of interleukin-6 (IL-6) during infection of mice with Listeria monocytogenes was investigated both in vitro and in vivo. Peritoneal cells taken at intervals from infected mice and cultured in vitro without added stimulus produced high titers of IL-6 peaking 2 days postinfection in a time course similar to that observed in vivo. Adherent cells with the morphology of macrophages were a major source of this IL-6. Spleen cells similarly harvested at intervals and cultured with heat-killed Listeria or heat-killed Brucella organisms as specific and nonspecific stimuli, respectively, showed two distinct IL-6 responses: (i) an early-phase response up to 5 days after infection when IL-6 production was elicited by either a specific or nonspecific stimulus, and when depletion of T cells had no effect, and (ii) a later response 7 to 10 days after infection when very high levels of IL-6 were produced in response to a specific stimulus. This response was lost when T cells were depleted in vitro or in vivo or in spleen cell cultures from mice with severe combined immunodeficiency. However, studies in vivo failed to show an important role for T cells governing serum IL-6. We conclude that most of IL-6 detected in vivo is produced by nonlymphocytes. Whether IL-6 produced by T lymphocytes in local foci of infection has any role in resolution of that infection is unknown.

Animals↗
PubMed1995

Organization and structure of actin filament bundles in Listeria-infected cells.

During its motion inside host cells, Listeria monocytogenes promotes the formation of a column of actin filaments that extends outward from the distal end of the moving bacterium. The column is constructed of short actin filaments that polymerize at the bacteria-column interface. To get a measure of filament organization in the column, Listeria grown in cultured PtK2 cells were studied with steady state fluorescence polarization, confocal microscopy, and whole cell intermediate voltage electron microscopy. Although actin filament ordering was higher in nearby stress fibers than in the Listeria-associated actin, four distinct areas of ordering could be observed in fluorescence polarization ratio images of bacteria: 1) the surface of the bacteria, 2) the cytoplasm next to the bacteria, 3) the outer shell of the actin column, and 4) the core of the column. Filaments were preferentially oriented parallel to the long axis of the column with highest ordering along the long axis of the bacterial surface and in the shell of the tail. The lowest ordering was in the core (where filaments are possibly also shorter with respect to the cup and the shell), whereas in the adjacent cytoplasm, filaments were oriented perpendicular to the column. A mutant of Listeria that can polymerize actin around itself but cannot move intracellularly does not have its actin organized along the bacterial surface. Thus the alignment of the actin filaments along the bacterial surfaces may be important for the intracellular movement. These conclusions are also supported by confocal microscopy and whole mount electron microscopic data that also reveal that actin filaments can be deposited asymmetrically around the long axis of the bacteria, a distribution that may affect the direction of motility of Listeria monocytogenes inside infected cells.

Actins↗
PubMed1998

Chronic Listeria infection in SCID mice: requirements for the carrier state and the dual role of T cells in transferring protection or suppression.

Listeriosis in mice with the SCID mutation results in a chronic infection. The chronic infection is characterized by abundant granulomas and neutrophil infiltrates. Both lesions were particularly noticeable in the liver. In the liver, about 95% are granulomas with 5% microabscesses involving intrahepatic infection. The majority of Listeria resided in membrane-bound vacuolar structures of the macrophages and not in the cytosol. Three manipulations resulted in alterations in the equilibrium between granulomas and liver microabscesses, with massive transfer of the infection to the hepatocyte and dissolution of the granulomas: depletion of neutrophils and neutralization of IFN-gamma and TNF-alpha. We did not find a role for IL-12, IL-10, or nitric oxide. Adoptive transfer studies showed a decisive role for both CD4+ and CD8+ T cells for an effective immune response, i.e., clearance of bacteria, granuloma formation with lymphocytes, and disappearance of microabscess. Clearance of Listeria was induced by transfer of CD8+ T cells from mice with targeted disruption of the IFN-gamma structural gene (IfgTM1KO), even in the presence of neutralizing mAb to IFN-gamma. In marked contrast, transfer of CD4+ T cells from IfgTM1KO mice exacerbated the infection in the chronically infected SCID mice, resulting in increased mortality with dissolution of the granulomas and severe hepatic infection with neutrophil infiltration. Thus, these data indicate that both IFN-gamma-dependent and -independent mechanisms are operative in the context of a chronic listerial infection.

Adoptive Transfer↗
PubMed1996

Lymphokine-activated killer cells lyse Listeria-infected hepatocytes and produce elevated quantities of interferon-gamma.

The bulk of Listeria monocytogenes injected intravenously into mice is taken up in the liver, where hepatocytes serve as the principal site of intracellular replication. NK cells have been implicated in host defenses to a variety of intracellular pathogens. To explore the role of NK cells in resistance to listerial infections of the liver, lymphokine-activated natural killer (LAK) cells were cocultured with Listeria-infected hepatocytes. The aspartate aminotransferase activity in the medium (evidence of cytotoxicity and hepatocyte damage) was elevated significantly in these cultures. Conversely, the viability of intracellular Listeria organisms was reduced. Increased quantities of interferon-gamma (IFN-gamma) were also detected. IFN-gamma production by LAK cells was modulated by interleukin (IL)-2 and IL-12. These findings suggest that the response of LAK cells to infected hepatocytes may play a critical role in host defenses to Listeria organisms taken up in the liver.

Animals↗
PubMed2000

Recombinant human interleukin-11 has anti-inflammatory actions yet does not exacerbate systemic Listeria infection.

To determine whether recombinant human (rh) interleukin (IL)-11 disrupts the clearance of microbial pathogens, mice were challenged with Listeria monocytogenes after receiving high-dose rhIL-11, anti-tumor necrosis factor (TNF) monoclonal antibody (MAb), anti-IL-11 MAb, or saline control. The LD50 was not affected by rhIL-11 but was 10-fold lower in the anti-TNF MAb group (P<.001). Plasma IL-6, IL-1beta, and TNF-alpha levels were not different between rhIL-11-treated animals and the control group; however, interferon-gamma levels were significantly reduced by IL-11 treatment (2477 vs. 0 pg/mL, P<.01). Compared with the control group, the quantitative level of L. monocytogenes in hepatic and splenic tissue was unchanged by rhIL-11 but was significantly increased by TNF or IL-11 inhibition. The results indicate that IL-11 down-regulates cytokine production but does not exacerbate systemic infection in the murine Listeria infection model.

Animals↗
PubMed2000

Innate defenses in the liver during Listeria infection.

The majority of pathogens entering the bloodstream are cleared by the liver. Listeria monocytogenes, an important natural pathogen of humans, is a useful tool for examining protective immune responses during systemic infections of mice. Innate immunity contributes to blood clearance and eventual sterilization of the liver subsequent to Listeria infections. Effector mechanisms expressed in the liver early after infections are orchestrated by complex interactions between resident populations, i.e. hepatocytes and Kupffer cells, with infiltrating monocytes, neutrophils, and natural killer cells. These interactions include cell to cell contact through adhesion molecules, as well as communication through secretion of cytokines and chemokines. The liver environment, as the interface between blood-borne pathogens and innate host defenses, is reviewed here.

Animals↗
PubMed2002

Tissue-level regulation of Th1 and Th2 primary and memory CD4 T cells in response to Listeria infection.

Ag-specific Th1 and Th2 cytokine-producing CD4 T cells were quantitated in secondary lymphoid and tertiary tissues following oral Listeria monocytogenes infection. Although the response to Listeria was previously believed to be predominantly Th1 like, CD4 T cells producing IL-4 or IL-5 comprised a substantial proportion of the overall primary and memory response. The frequency of IFN-gamma-, IL-4-, or IL-5-producing primary effector or memory CD4 T cells was significantly higher in lung, liver, and intestinal lamina propria (LP) as compared with spleen and lymph node. However, maximum numbers of IL-4- and IL-5-producing cells were detected in the LP several days after the peak of the Th1 response, and IL-5 production was skewed toward the mucosal tissues. Remarkably, the recall response resulted in sustained Th1 and Th2 responses in tertiary, but not lymphoid tissues and long-term retention of Th1 and Th2 memory cells in equal proportions in the LP. Finally, CD40 ligand was essential for induction of IFN-gamma in the spleen and LP, but not in the liver and lung, while the IL-4 response required CD40 ligand only in the spleen. Therefore, the rules governing the effector phenotype, and the overall magnitude of the CD4 response, are regulated at the level of individual tissues.

Animals↗
PubMed2005

Listeria-infected myeloid dendritic cells produce IFN-beta, priming T cell activation.

The intracellular bacterium Listeria monocytogenes infects dendritic cells (DC) and other APCs and induces potent cell-mediated protective immunity. However, heat-killed bacteria fail to do so. This study explored whether DC differentially respond to live and killed Listeria and how this affects T cell activation. To control for bacterial number, a replication-deficient strain, Lmdd, defective in D-alanine biosynthesis, was used. We found that DC internalize both live and heat-killed Lmdd and similarly up-regulate the expression of costimulatory molecules, a necessary step for T cell activation. However, only live Lmdd-infected DC stimulate T cells to express the early activation marker CD69 and enhance T cell activation upon TCR engagement. Infection with live, but not heat-killed, Lmdd induces myeloid DC to secrete copious amounts of IFN-beta, which requires bacterial cytosolic invasion. Exposure to high concentrations of IFN-beta sensitizes naive T cells for Ag-dependent activation.

Animals↗
PubMed1988

Pathology of Listeria infection in murine severe combined immunodeficiency. A study by immunohistochemistry and electron microscopy.

Mice bearing the scid mutation lack functional T and B lymphocytes and partially resist infection with the intracellular pathogen Listeria monocytogenes. In this study, we describe the histopathologic features of the infection in scid mice. Infected scid showed hyperplasia of mononuclear cells in lymphoid organs without any evidence of granulomas nor of lymphoid cell development. Mononuclear phagocytes in various tissues of infected scid mice had markedly enhanced expression of class II histocompatibility molecules (or Ia molecules). Furthermore, Ia expression was also found in endothelial and epithelial cells of many organs in the later stages of infection. These results confirm that scid mice have a mechanism for activation of Ia antigen expression, which is independent of lymphocyte function.

Animals↗