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PubMed1995

Early appearance of T cell receptor alpha beta + CD4- CD8- T cells with a skewed variable region repertoire after infection with Listeria monocytogenes.

We found that the number of T cell receptor (TCR) alpha beta + CD4- CD8- T cells increased in the peritoneal cavity on day 5 after an intraperitoneal infection with Listeria monocytogenes strain EGD together with TCR gamma delta + CD4- CD8- T cells. Thereafter, the TCR alpha beta + CD4- CD8- T cells decreased to a normal level by day 14. The TCR alpha beta + CD4- CD8- T cells showed an activated T cell phenotype (L-selectin CD44 +) and expressed CD45/B220 and interleukin-2 receptor beta, but did not express heat stable antigen, which is expressed by the immature CD4- CD8- thymocytes. Furthermore, 20-30% of the TCR alpha beta + CD4- CD8- T cells expressed the NK1.1 natural killer cell marker. Analysis of the TCR V region repertoire of the TCR alpha beta + CD4- CD8- T cells induced by L. monocytogenes infection showed that more than 80% of the TCR alpha beta + CD4- CD8- T cells expressed TCR V beta 8 detected by anti-TCR V beta 8.1 and 8.2 mAb, and a reverse transcription-polymerase chain reaction analysis of V alpha 14 relative to V alpha 11 expression revealed that the TCR alpha beta + CD4- CD8- T cells expressed a higher level of V alpha 14, which was reported to be preferentially expressed by TCR alpha beta + CD4- CD8- thymocytes rather than conventional CD4+ T cells. The TCR alpha beta + CD4- CD8-T cells showed a proliferative response to anti-TCR alpha beta mAb stimulation. In contrast, they showed no response to stimulation with either Listeria antigen or 65-kDa heat shock protein of Mycobacterium bovis, which do stimulate the Listeria-specific TCR alpha beta + CD4- CD8- T cells and the Listeria-induced TCR gamma delta + T cells, respectively. These results suggest that the TCR alpha beta + CD4- CD8- T cells may recognize a restricted set of self antigens induced by L. monocytogenes infection, and that they contribute to host protection at an early stage of infection.

Animals↗
PubMed1994

Recombinant interleukin-12 enhances resistance of mice to Listeria monocytogenes infection.

The effect of recombinant murine IL-12 (rIL-12) or anti-IL-12 antibody administration on resistance to murine listeriosis was investigated. Mice given a single 0.5 micrograms dose of rIL-12 had 1.5 log10 fewer listeriae in their spleens and livers as compared with control infected mice 3 days after L. monocytogenes challenge. Conversely, administration of anti-IL-12 IgG caused an equivalent increase in the cfu of L. monocytogenes recovered from the spleens and livers as compared to control mice. This is the first report of such a protective effect from a single dose of rIL-12. Treatment of uninfected mice with rIL-12 induced IFN-gamma mRNA production in their livers. Infection of mice with L. monocytogenes caused a similar increase in IFN-gamma mRNA levels that was not increased further by concurrent treatment with rIL-12. Treatment of mice with an anti-IFN-gamma MAb eliminated the protective effect of IL-12 on Listeria infection. Expression of TNF-alpha, IL-10 and IL-12p40 mRNA in L. monocytogenes-infected mice were not significantly altered by administration of either anti-IL-12 IgG or rIL-12. rIL-12 administration was associated with increased serum AST levels, a measure of liver damage, 1 day after treatment in L. monocytogenes-infected mice. In addition, rIL-12 administration was associated with the increased presence of small inflammatory foci and necrotic hepatocytes in both infected and uninfected mice, suggesting a proinflammatory role for IL-12 in the liver.

Animals↗
PubMed1989

Protective effect of N-acetyl chitohexaose on Listeria monocytogenes infection in mice.

A water-soluble oligosaccharide, N-acetyl chitohexaose (NACOS-6) was able to enhance the protecting effect of BALB/c male mice against Listeria monocytogenes infection, when administered intraperitoneally 24 hr before the challenge with this microbe. Significant decrease in number of microbes within the peritoneal cavity, spleen, and liver from the mice of NACOS-6-administered group was not observed 1 day after the infection but 4 days after the infection. Administration of NACOS-6 enhanced the delayed-type hypersensitivity response against sheep red blood cells (SRBC) or heat-killed L. monocytogenes. Splenic T lymphocytes from mice administered NACOS-6 released macrophage activating factor (MAF). These results suggested that NACOS-6 was also able to elevate the function of cellular immunity. Macrophages treated with a combination of NACOS-6 and the culture supernatant of splenic T lymphocytes from mice administered NACOS-6, "NACOS-6 sup," were found to exert a fairly strong growth-inhibitory effect on L. monocytogenes. Interferon-gamma (IFN-gamma) and interleukin 2 (IL-2) were able to enhance the growth-inhibitory effect on L. monocytogenes by the NACOS-6-treated macrophages.

Animals↗
PubMed1985

Sequential production of alpha and beta interferons and gamma interferon in the circulation of Listeria monocytogenes-infected mice after stimulation with bacterial lipopolysaccharide.

Sequential production of interferon (IFN)-alpha/beta and IFN-gamma in the circulation of mice which had been previously infected with viable Listeria monocytogenes was induced by injection of lipopolysaccharide (LPS) derived from Salmonella typhimurium. IFN-alpha/beta production occurred 2 hr after injection of LPS, thereafter IFN-gamma appeared and the maximum titer was demonstrated at 6 hr. At that time, almost all of the IFN was IFN-gamma. IFN-gamma production in response to LPS was observed from the 5th through the 11th day after infection with Listeria, but it was not demonstrated in either mice infected with lower doses of viable Listeria or mice immunized with heat-killed bacteria. IFN-alpha/beta production was not drastically affected by treatment with hydrocortisone, cyclophosphamide, carrageenan, antithymocyte serum, or anti-asialo GM1 antibody, whereas IFN-gamma production was suppressed by administration of all those agents. Noteworthily, IFN-alpha/beta, but not IFN-gamma, was produced even 6 hr after stimulation with LPS in cyclophosphamide- or antithymocyte serum-treated mice. IFN-gamma induction by LPS was markedly suppressed in mice in which IFN-alpha/beta produced by Listeria infection itself had been depleted by treatment with anti-mouse IFN-alpha/beta antibody, but it was not inhibited in mice when IFN-alpha/beta induced not by Listeria infection but by LPS had been depleted by treatment with anti-mouse IFN-alpha/beta antibody.

Animals↗
PubMed2002

[Effects of aluminum ions on the resistance of mice to experimental Listeria monocytogenes infection].

This study presents evaluation of effects of aluminium ions on the development of experimental infection induced by the injection of Listeria monocytogenes bacteria into growing mice. We show that single exposure of mice to 0.05 LD50 or 0.5 LD50 of aluminium ions does not affect the accumulation of bacteria in liver and spleen of experimental animals. Long-term exposure of mice to aluminium ions (injection of 0.05 LD50 Al3+ every 3 days for totally 6 weeks) did not slow down the increase in weight of animals while in the infected animals aluminium significantly reduced their growth. Animals subjected to chronic aluminium exposure have shown lower accumulation of bacteria in liver 24 h after the initiation of experimental infection as compared to the mice after single injection of 0.05 LD50 Al3+. Also, long-term exposure to aluminium causes more complicated development of experimental infection, which was evidenced by the decreased survival of aluminium-treated animals (77% compared to 83% in control group) as well as by the increase in the fraction of animals carrying infection after 6 weeks (36% versus 5% in control group). In addition, aluminium-exposed animals had significantly lower blood serum agglutination titer to the listeria, and decrease in the delayed type of hypersensitivity to the listeria antigens. Results, presented here, indicate that the long-term exposure to low aluminium doses activates the antibacterial defence in experimental animals while the specific immunity becomes suppressed.

Aluminum↗
PubMed2004

Changes in peritoneal myeloid populations and their proinflammatory cytokine expression during infection with Listeria monocytogenes are altered in the absence of gamma/delta T cells.

Evidence that gamma/delta T cells play a broad, immunoregulatory role has been accumulating steadily. We show here that myeloid cells are disregulated after peritoneal infection with Listeria monocytogenes in mice lacking gamma/delta T cells. Inflammatory populations of neutrophils and monocytes recruited to the site of infection remained longer. Intracellular cytokine analysis showed that frequencies of myeloid cells producing interleukin-12 and tumor necrosis factor alpha were higher and remained elevated longer after infection in mice genetically deficient in gamma/delta T cells. In vivo dye-tracking studies indicated that the majority of inflammatory monocytes differentiated into resident tissue macrophages in situ. In vitro experiments confirmed that monocytes harvested from mice lacking gamma/delta T cells were defective in their maturation process. This evidence suggests that gamma/delta T cells promote differentiation in the monocyte/macrophage lineage. These cells are important for bactericidal activity, inflammatory cytokine production, clearance of inflammatory neutrophils, and ultimately, antigen presentation to T cells. Regulation of monocyte/macrophage differentiation may underlie a broad segment of the phenotypic alterations that have been reported in mice lacking gamma/delta T cells.

Animals↗
PubMed1977

Cell-mediated resistance to infection with Listeria monocytogenes in nude mice.

Congenitally dysthymic nude (nu/nu) NMRI mice showed increased resistance to viable Listeria monocytogenes cells during the initial phase of infection as compared with euthymic control mice. The intravenous mean lethal dose (LD50), as determined for euthymic mice after an observation time of 7 and 14 days, amounted consistently to 6 X 10(4) Listeria. The corresponding values determined in nude mice were found to be increased by either 20-fold (1.2 X 10(6) Listeria after an observation time of 7 days) or 4-fold (2.4 X 10(5) Listeria after an observation time of 14 days). The transfer of spleen cells from immune euthymic donor mice into chronically infected nude mice caused almost complete elimination of Listeria within 1 week. The injection of dextran sulfate 24 h before a secondary infection with L. monocytogenes caused loss of antibacterial resistance in both chronically infected nude mice and Listeria-immune euthymic mice, this being expressed by a rapid increase in the numbers of bacteria in the spleens as well as the occurrence of serious signs of illness.

Animals↗
PubMed1997

Listeria monocytogenes infection of P388D1 macrophages results in a biphasic NF-kappaB (RelA/p50) activation induced by lipoteichoic acid and bacterial phospholipases and mediated by IkappaBalpha and IkappaBbeta degradation.

As previously reported, Listeria monocytogenes infection of P388D1 macrophages results in a rapid induction of NF-kappaB DNA-binding activity. Here we show that this induction of NF-kappaB activity occurs in a biphasic mode: first, a transient, IkappaBalpha degradation-dependent phase of activity, also induced by the nonvirulent species Listeria innocua, which is mediated by binding of the bacteria to the macrophage, or by adding Listeria-derived lipoteichoic acid to the macrophage; the second persistent phase of activation is only markedly induced when the bacteria enter the cytoplasm of the host cell and express the virulence genes plcA and plcB, encoding two phospholipases. We suggest that products of the enzymatic activity of phospholipases directly interfere with host cell signal transduction pathways, thus leading to persistent NF-kappaB activation via persistent IkappaBbeta degradation.

Animals↗
PubMed1997

Listeria monocytogenes infection of HeLa cells results in listeriolysin O-mediated transient activation of the Raf-MEK-MAP kinase pathway.

In this study we investigated the effect of Listeria monocytogenes infection on the activation of the Raf-MEK-MAP kinase pathway in eukaryotic host cells. HeLa cell infection with L. monocytogenes EGD resulted in a rapid, but transient, phosphorylation of the MAP kinases erk-1 and erk-2, a transient phosphorylation of the MAP kinase kinase MEK-1, and a transient activation of the MAP kinase kinase kinase Raf. In parallel to the transient phosphorylation of the MAP kinases, we detected induced expression of the MAP kinase phosphatase MKP-1. Additionally we present evidence that listeriolysin O is the inducing agent for activation of the Raf-MEK-MAP kinase pathway.

Bacterial Toxins↗
PubMed1995

A monoclonal antibody against T-cell receptor alpha beta induces endogenous cytokines and prevents mice from a lethal infection with Listeria monocytogenes.

In vivo induction of cytokines by a monoclonal antibody (mAb) against T-cell receptor (TCR) alpha beta and the protective effect induced by the mAb on a lethal infection with Listeria monocytogenes were studied. Injection of anti-TCR alpha beta mAb induced rapid production of endogenous tumour necrosis factor in the spleens, and gamma interferon and interleukin-6 in the blood streams and spleens of mice. Administration of anti-CD4 mAb, anti-CD8 mAb, or anti-Thy1.2 mAb resulted in suppression of anti-TCR alpha beta mAb-induced endogenous cytokine production. Mice were protected against lethal L. monocytogenes infection when treated with anti-TCR alpha beta mAb. The protective effect was not demonstrated in CD4+ cell- or CD8+ cell-depleted mice. These results suggest that anti-TCR alpha beta mAb shows a protective effect on a lethal infection with L. monocytogenes in mice and that the mAb-induced endogenous cytokines might be involved in the effect of anti-TCR alpha beta mAb.

Animals↗
PubMed1973

Effects of antithymocyte and antimacrophage sera on the survival of mice infected with Listeria monocytogenes.

Antisera prepared in rabbits against purified mouse thymocytes (antithymocyte serum; ATS) and peritoneal macrophages (antimacrophage serum; AMS) were injected intraperitoneally into Balb/c mice infected with the bacterium Listeria monocytogenes. When administered near the initiation of infection, the ATS significantly decreased the survival time of the animals and increased the mortality rate. When ATS was administered 6 days after a sublethal dose of L. monocytogenes had been inoculated, an overt disease did not evolve. ATS that significantly potentiated primary listeriosis also had high cytotoxicity titers for thymocytes and lymphoid cells from the peritoneal cavity. Although cytotoxic activity against peritoneal macrophages could be demonstrated in lower dilutions of the ATS, this activity did not appear to correlate with the effects of the sera on listeriosis. The injection of AMS did not enhance the infectious process. In some trials more deaths occurred among mice receiving normal rabbit serum than those receiving AMS. All of the AMS had cytotoxic titers against peritoneal macrophages, and the sera were usually inactive against thymocytes and peritoneal lymphoid cells. Listeria was isolated from fatally infected mice with nearly equal success in all of the serum-treated groups, and the serum treatments did not appear to alter the pattern of gross lesions. The afferent limb of the immune response was markedly affected by the presence of antibodies to lymphocytes. However, antibodies reacting with macrophages did not demonstrably enhance the Listeria process, which depends upon cellular immunity as the principal means of acquired host defense.

Animals↗
PubMed2000

Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infection.

Various bacterial pathogens have been identified as mediators of apoptosis. Apoptosis reportedly shows both detrimental and beneficial effects on biological functions. We studied the role of liver apoptosis in lethal Listeria monocytogenes infection and the regulation of apoptosis by endogenous cytokines during infection. Apoptosis was observed in the spleen but not in the liver of infected mice, whereas the induction of liver necrosis was evident by rising levels of serum aminotransferases in these animals. Apoptosis was detected in the liver of L. monocytogenes-infected mice which had been treated with monoclonal antibody (mAb) against tumor necrosis factor-alpha (TNF-alpha) or interleukin-6 (IL-6), or in TNF-alpha(-/-) mice, but not in gamma- interferon (IFN-gamma)(-/-) mice or mice which had been treated with mAb against IL-4 or IL-10. Augmentation of liver apoptosis in mice treated with mAb against TNF-alpha or IL-6 or in TNF-alpha(-/-) mice correlated with the increase in bacterial numbers in the organ, while no augmentation of apoptosis was observed in the liver of IFN-gamma(-/-) mice irrespective of the marked increase in bacterial numbers in the organs, indicating that augmentation of liver apoptosis may not be merely due to the increase in bacterial growth in the organs. These results suggest that TNF-alpha and IL-6 may play an important role in protecting the liver from apoptosis in lethal L. monocytogenes infection.

Animals↗
PubMed1978

[Influence of killed Bordetella pertussis cells on the resistance against infection with Listeria monocytogenes (author's transl)].

The influence of killed Bordetella pertussis cells (B.p.) on the cell-mediated resistance of mice against infection with virulent germs of Listeria monocytogenes has been studied. Resistance of mice was decreased, when 3 X 10(9) B.p. were injected 1 day before, simultaneously with or 1 day after infection, resulting in augmented amounts of viable Listeriae recovered from the spleens 3 days after infection (figure 1). The LD50 was strongly reduced (Table 1). Transfer of immune spleen cells to recipient mice, which had been treated 1 day previously with 3 X 10(9)B.p., did not support resistance definitely (Table 2). Therefore, it can be concluded that probably the macrophage system was impaired just after B.p. injection. When, however, B.p. were given several days before infection, resistance was increased. A maximum of resistance enhancement was seen 7-14 days after B.p. treatment. Thereafter, this beneficial effect gradually decreased but persisted for at least 67 days (figure 1). This resistance enhancing effect of B.p. was surely not due to adjuvant effect of B.p. on the T-lymphocyte-mediated immune reaction to Listeriae, since in B.p.-pretreated mice the development of immunity during the primary infection to a secondary listeric infection has even been lacking (Table 3). It is more likely that the macrophage system was stimulated at this time by B.p. In mice treated 7 days prior to infection the elimination of Listeriae from the spleens was supported from the very beginning of the infection (figure 2).

Adjuvants, Immunologic↗
PubMed2005

Omega-3 polyunsaturated fatty acid impairment of early host resistance against Listeria monocytogenes infection is independent of neutrophil infiltration and function.

The primary objective of this study was to determine whether the n-3 PUFA-mediated changes in host response to a Listeria monocytogenes infection (e.g., cytokine production and bacterial clearance) were dependent upon neutrophils. Balb/c mice were fed one of two semi-purified diets that contained either 0 or 41 g of n-3 PUFA/kg. After 4 week, mice were injected with a neutrophil-depleting (RB6-8C5) or isotype-control antibody 24 h prior to infection. Bacterial clearance from the liver and spleen at 3 days post-challenge was measured and the concentration of five pro-inflammatory cytokines in sera 24 h post-infection were determined using a novel protein multiplexing kit. We found that neutrophil depletion impaired bacterial clearance independent of the effect of n-3 PUFA. Interestingly, we observed a rather complex interaction between neutrophil-depletion and n-3 PUFA intake on in vivo pro-inflammatory cytokine production. For example, neutrophil depletion elevated circulating IL-6 and MCP-1 (2- to 5-fold; p<0.05) in n-3 PUFA-fed mice, but less so or not at all in mice fed the control diet. In summary, our data suggest that n-3 PUFA-mediated reduction of host resistance to L. monocytogenes is independent of neutrophil activity.

Animals↗
PubMed1987

Depression of murine hepatic mixed function oxidase during infection with Listeria monocytogenes.

The level of cytochrome P-450 and the oxidation of aminopyrine and benzo(a)pyrene hydroxylase were depressed in hepatic microsomes prepared from mice infected with the gram positive bacteria Listeria monocytogenes. Maximum depression of mixed function oxidase occurred on the 2nd day of infection. This loss in drug biotransformation capacity in the liver was correlated directly with the number of organisms found in that organ. The ability of mice to metabolize drugs in vivo also was impaired during Listeria monocytogenes infection. During the infective period the half-life of theophylline was significantly prolonged and the N-demethylation of aminopyrine as measured by the expiration of 14CO2 from radiolabeled aminopyrine was diminished. The loss of drug metabolism was not due to interferon production, fever or morphological damage to the liver. These results indicate that certain bacterial infections can depress drug biotransformation and elimination in a similar manner to that already reported in viral and parasitic infections. This finding may be of significance to patients receiving drugs which are metabolized by the mixed function oxidase system during episodes of infection with some bacteria.

Aminopyrine N-Demethylase↗
PubMed1995

Detection of anti-listeriolysin O in dairy cattle experimentally infected with Listeria monocytogenes.

A dot-blot assay and an enzyme-linked immunosorbent assay (ELISA) to detect listeriosis in dairy cattle were developed that detected anti-listeriolysin O antibodies in the serum of cows experimentally infected with Listeria monocytogenes. The tests utilized purified listeriolysin O (LLO) as the detection antigen and streptolysin O (SLO) to absorb cross-reacting antibodies. The two tests were compared with an agglutination test that used formalin-killed whole L. monocytogenes cells. Blood samples were collected periodically from 17 cows after intramammary gland infection, and the development of anti-LLO antibodies was followed by an agglutination test, the dot-blot test, and the ELISA. In general, an agglutination titer of > 640 was needed for a positive dot-blot anti-LLO test for nonpregnant cows. However, 1 pregnant cow with an agglutination titer of 20 was positive in the dot-blot test. The ELISA was as sensitive as the dot-blot assay but gave a quantitative measurement to distinguish serum samples of positive reactors from cross-reactors. The specificity of the LLO-based tests was further evaluated using serum from cows that had been experimentally infected with Staphylococcus aureus, 17 of which had agglutination titers for L. monocytogenes > 640. These elevated agglutination titers were probably due to cross-reacting bacterial antigens because serum from 9 of 17 of these animals did not react to the purified LLO antigen. A positive response to the LLO-based dot-blot and ELISA assays is indicative of previous or current infection with L. monocytogenes.

Agglutination Tests↗