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PubMed1993

Characterization of T-cell receptor gamma delta T cells appearing at the early phase of murine Listeria monocytogenes infection.

It has been shown that T-cell receptor (TcR) gamma delta + CD4- CD8- T cells increase in number and have an important role in early protection in murine Listeria monocytogenes infection. In this report, to characterize further the phenotype of the gamma delta T cells in listeriosis, we analysed V region gene usage and in vitro antigen recognition of the TcR gamma delta T cells in the peritoneal cavity of mice at the early phase after i.p. infection with a sublethal dose of L. monocytogenes. The gamma delta T cells predominantly expressed V delta 6 which has been reported to be expressed by TcR gamma delta-bearing foetal thymocyte hybridomas specific to mycobacterial and self heat-shock protein (hsp) 60. These early appearing CD3+ CD4- CD8- T cells in Listeria-infected mice, which were reported to be TcR gamma delta T cells, increased in proportion and in size by in vitro stimulation with recombinant hsp 60 from Mycobacterium bovis and purified protein derivative from M. tuberculosis but not by stimulation with heat-killed L. monocytogenes. A 65,000 MW molecule was detected in the lysate of viable L. monocytogenes but not in the lysate of heat-killed L. monocytogenes by a monoclonal antibody (mAb) raised against mycobacterial hsp 60. These results suggest that the V delta 6-bearing peripheral gamma delta T cells are activated by recognizing listerial hsp 60 expressed by viable L. monocytogenes. The hsp 60-reactive V delta 6-bearing T cells may have an important role in protection against L. monocytogenes and other parasites that express hsp 60 at high level.

Animals↗
PubMed1996

[Two cases of Listeria monocytogenes infection in Osaka Municipal Hospital].

We report two cases of sepsis and meningoencephalitis with listeriosis. They died in despite of administering sensitive antibiotics. A 2 day old girl was admitted to our hospital because of fever and cyanosis. Listeria monocytogenes type 4b was cultured from blood, CSF, throat, urine, ear. She was treated with twice exchange transfusion and sensitive antibiotics (ABPC, TOB), but died from DIC. A 48 year old man suddenly experienced an unconscious condition. A CSF culture grew L. monocytogenes type 1/2a. He was treated with sensitive antibiotics (ABPC, CEZ etc), but went bad conditions. Listeria infection of this cases developed as unfortunate infection.

Female↗
PubMed1994

Influence of antiorthostatic suspension on resistance to murine Listeria monocytogenes infection.

The present study was designed to evaluate the influence of antiorthostatic suspension, a ground-based modeling system employed to simulate certain aspects of weightlessness that occur during space flight, on the capacity of mice to resist infection with the facultative intracellular bacterial pathogen Listeria monocytogenes. Female BDF1 mice were suspended by the tail in the orthostatic or antiorthostatic position and were infected with a sublethal dose of virulent L. monocytogenes at various times during the suspension. It was found that suspension did not influence the kinetics of bacterial growth in vivo if the infection was started concurrently with the suspension. However, mice that were antiorthostatically suspended 2, 4, or 7 days before the onset of infection exhibited an enhanced capacity to eliminate the challenge infection. Suspending mice on day 2 of the infection did not alter the kinetics of bacterial growth. Finally, the enhancement of resistance to the primary Listeria infection was accompanied by failure of the mice to generate long-term protective immunological memory to the challenge organism. Collectively, these results indicate that the stress of antiorthostatic suspension can influence the capacity of mice to resist bacterial infection.

Animals↗
PubMed1998

Differential chemokine response of murine macrophages stimulated with cytokines and infected with Listeria monocytogenes.

During inflammatory processes the infected macrophage is a rich source of chemokines which induce infiltration of leukocytes to the site of infection. We investigated the regulation of chemokine production by murine macrophages in response to infection with the intracellular bacterial pathogen, Listeria monocytogenes. As a source of quiescent macrophages, murine bone marrow-derived macrophages (BMM) cultured under serum-free conditions were used. With RT-PCR, we detected induction of RNA message for the chemokines macrophage inflammatory protein (MIP)-2, KC, MIP-1alpha, MIP-1beta, IFN-gamma-inducible protein-10 and RANTES in L. monocytogenes-infected macrophages. Accordingly, ELISA-detectable MIP-1alpha, MIP-2 and KC protein was induced by infection with L. monocytogenes. In contrast, L. monocytogenes infection of BMM alone failed to induce considerable expression of monocyte chemoattractant protein (MCP)-1 at the mRNA or protein level, but co-treatment with IFN-gamma was necessary. Release of infection-triggered MIP-2, MIP-1alpha and KC was negatively regulated by IFN-gamma. Similarly, IL-4 stimulated MCP-1 release by infected macrophages but reduced production of MIP-1alpha, MIP-2 and KC. IL-10 turned out to be a general deactivator in terms of macrophage chemokine production. IL-13 had no effect on MIP-1alpha, MIP-2 and KC production by infected BMM, but slightly reduced MCP-1 release. By using IFN-gamma and IL-4 gene deletion mutant mice, in vivo regulation of these chemokines by IL-4 and IFN-gamma in listeriosis was studied. In summary, our results show that chemokines are produced by macrophages infected with L. monocytogenes, and that chemokine release is differentially regulated by the macrophage modulators IFN-gamma, IL-4, IL-10 and IL-13.

Animals↗
PubMed2005

Lentinan has a stimulatory effect on innate and adaptive immunity against murine Listeria monocytogenes infection.

Lentinan, a (1-3)-beta glucan from Lentinus edodes, is licensed as an immunostimulatory drug. We tested the effect of lentinan in the well-established model system of the murine Listeria monocytogenes infection. Pre-treatment of bone marrow macrophages and dendritic cells with lentinan resulted in increased production of TNF-alpha and IL-12 after L. monocytogenes infection in vitro. After lentinan treatment bone marrow macrophages showed increased NO-production and enhanced cytotoxic activity against L. monocytogenes. Pre-treatment of mice with lentinan resulted in increased concentrations of TNF-alpha, IL-12 and IFN-gamma and also an increased number of L. monocytogenes specific CD8 T cells in the spleen. The bacterial burden in spleen and liver of mice was significantly reduced during primary and secondary Listeria infection after lentinan pre-treatment of mice. In summary these results show that lentinan enhances the protective CD8 T-cell response against L. monocytogenes probably by a mechanism that involves the IL-12-mediated augmentation of the specific antilisterial CD8 T-cell response.

Adjuvants, Immunologic↗
PubMed1996

Interferon-gamma and interleukin-10 have cross-regulatory roles in modulating the class I and class II MHC-mediated presentation of epitopes of Listeria monocytogenes by infected macrophages.

IFN-gamma is an important cytokine in resistance to infection with Listeria monocytogenes, and interleukin 10 is known to exacerbate infection with Listeria and other intracellular pathogens. We examined the effects of these cytokines on antigen presentation by macrophages infected with live Listeria. Listeriolysin O, a hemolysin secreted by Listeria, is an immunodominant antigen presented by both class I and class II MHC on infected cells. Thioglycollate-elicited macrophages were pretreated with exogenous IFN-gamma, IL-10, or both cytokines overnight, infected with bacteria, and then fixed. Epitope-specific, MHC-restricted, T cell hybridomas were then added to detect the presentation of the class I or class II ligand. We found that IFN-gamma enhanced the presentation of both the class I and class II epitopes and IL-10 strongly inhibited the presentation of both ligands. The degree of inhibition of presentation caused by IL-10 was dose dependent. IL-10 was also able to inhibit the presentation of exogenously added class II-binding peptide but had a less dramatic effect on the presentation of the added class I-binding polypeptide epitope. Flow cytometric analysis of expression of class I and class II on treated macrophages demonstrated that the inhibitory effect of IL-10 on antigen presentation was not due to significant downregulation of MHC expression. This loss of antigen presentation was also not due to downregulation of the costimulatory molecule, B7-2. We have found that IFN-gamma and IL-10 have opposing immunoregulatory effects on the presentation of antigens derived from an intracellular pathogen and that the class I vs. class II-mediated presentation of antigens is differentially regulated by IL-10.

Animals↗
PubMed1986

Immunomodulatory effect of Listeria monocytogenes infection. III. Expression of Fc receptor and antibody-mediated cytotoxicity in infected mice.

The level of cells expressing Fc receptor and their ability to antibody mediated cytotoxicity was determined in this study. The adherent cells fraction isolated from blood leukocytes, splenocytes and peritoneal cells of Listeria monocytogenes infected Balb/c mice were rosetted with Ab-SRBC or SRBC. Moreover, blood leukocytes, splenocytes and peritoneal cells were incubated with Ab-51Cr SRBC and 51Cr SRBC as target cells and their cytotoxic activity was assessed by the per cent of specific 51Cr release. The results indicate that in the Listeria infected organisms the level of cells rosetting with Ab-SRBC is greatly increased particularly in peritoneal cells between the 3rd and 7th day of infection i.e. in the period of intensive production of macrophages. Only peritoneal cells exhibit the antibody dependent cytotoxicity. However, the intensity of this cytotoxicity does not correlate with the level of cells expressing Fc receptor.

Animals↗
PubMed1992

A protective role of gamma/delta T cells in primary infection with Listeria monocytogenes in mice.

We have previously reported that T cells bearing T cell receptors (TCRs) of gamma/delta type appear at a relatively early stage of primary infection with Listeria monocytogenes in mice. To characterize the early-appearing gamma/delta T cells during listeriosis, we analyzed the specificity and cytokine production of the gamma/delta T cells in the peritoneal cavity in mice inoculated intraperitoneally with a sublethal dose of L. monocytogenes. The early-appearing gamma/delta T cells, most of which were of CD4-CD8- phenotype, proliferated and secreted IFN-gamma and macrophage chemotactic factor in response to purified protein derivative from Mycobacterium tuberculosis, or recombinant 65-kD heat-shock protein derived from M. bovis but not to heat-killed Listeria. To further elucidate the potential role of the gamma/delta T cells in the host-defense mechanism against primary infection with Listeria, we examined the effects of in vivo administration of monoclonal antibodies (mAbs) against TCR-gamma/delta or TCR-alpha/beta on the bacterial eradication in mice infected with Listeria. Most of alpha/beta T cells or gamma/delta T cells were depleted in the peripheral lymphoid organs at least for 12 d after an intraperitoneal injection of 200 micrograms TCR-alpha/beta mAb or 200 micrograms TCR-gamma/delta mAb, respectively. An exaggerated bacterial multiplication was evident at the early stage of listerial infection in the gamma/delta T cells-depleted mice, whereas the alpha/beta T cell-depleted mice exhibited much the same resistance level as the control mice at this stage although the resistance was severely impaired at the late stage after listerial infection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Primary immune response of mice to sheep erythrocytes during the course of infection with Listeria monocytogenes.

The influence of an infection with a sublethal dose of viable Listeria monocytogenes on the primary antibody-forming potential of mice against sheep erythrocytes (SE) was monitored by means of counting plaque-forming cells (PFC) in the spleen and measuring circulating antibodies against SE. Additionally, the course of infection was followed by determination of viable bacteria in the spleen. As against the injection of killed L. monocytogenes, infection with viable bacteria did not display any significant influence on the immune response against SE when the immunogenic stimulus was given either stimultaneously with the bacteria or on day 4 or 13 of infection, respectively. Vice versa, the immunization with the particulate antigen had no measurable influence on either course of outcome of infection with the parasite.

Adjuvants, Immunologic↗
PubMed1983

[Antibiotic therapy in the compromised host--presented as a model for listeriosis in the mouse. II. Effect of tetracycline].

The effectiveness of tetracycline therapy on Listeria-infection in compromised host was evaluated in three different murine models. In normal adult mice infected with a tetracycline susceptible strain of Listeria monocytogenes, treatment with this antibiotic caused a reduced rate of multiplication of bacteria. That is, a low bacterial count was found in the spleen. When the macrophage system which in Listeria-infection represents a major defense mechanism was blocked through dextran sulfate 500, treatment with tetracycline was still very effective. In this case, bacterial multiplication has ceased. However, an elimination of the organisms could only be achieved after the macrophage system recovered from its temporary blockade. Secondly, nude athymic mice which are unable to develop cell mediated immunity were used to establish chronic infection with Listeria. Treatment with tetracycline in this instance only reduced bacterial counts moderately. Thirdly, five days old baby mice which are extremely susceptible to Listeria could at least partially be protected with tetracycline therapy against fatal infection.

Animals↗
PubMedDate not supplied

Rapidly enlarging iliac aneurysm secondary to listeria monocytogenes infection: a case report.

Infected aneurysms caused by Listeria monocytogenes are rare. Worldwide, 16 cases have been reported, none in the iliac system. The authors report the case of an 80-year-old man being followed for small aortic and right common iliac artery (RCIA) aneurysms who presented with progressive gastrointestinal symptoms. Serial computed tomography demonstrated a 200% increase in RCIA diameter with development of infection over 1 month. Right axillobifemoral bypass and aneurysm resection were performed. The authors believe this case represents the first description of bacteremic seeding of an iliac degenerative aneurysm by Listeria monocytogenes. The natural history and aggressive course of vascular infection with this organism are documented.

Aged↗
PubMed1987

Transfer of resistance to primary infection of Listeria monocytogenes and early induction of delayed hypersensitivity by sera from L. monocytogenes-infected mice.

We found a new phenomenon which differs from previous reports on experimental listeriosis, that is, failure of passive transfer of serum from Listeria monocytogenes-infected mice to convey resistance to the bacterium. Transfer of immune serum from L. monocytogenes-infected mice markedly augmented resistance to the bacterium, and mechanisms of the transfer of L. monocytogenes-immune serum were investigated. Transfer of immune serum prevented L. monocytogenes lethality. This effect of the immune serum was transferred dose dependently. Augmentation of resistance to L. monocytogenes also appeared in elimination of bacteria from the spleen. The growth of bacteria within 2 days in the spleen was not inhibited. Transfer of the immune serum augmented and accelerated induction of a delayed footpad reaction. Delayed hypersensitivity-dependent accumulation of mononuclear cells, detected by focus formation reaction in the liver, was also augmented. In contrast, polymorphonuclear cell accumulation in the liver was suppressed. Development of delayed hypersensitivity reactions was correlated with the elimination of bacteria in the spleens. These effects of the immune serum were expressed antigen specifically; however, the effector molecule(s) in the immune serum differs from immunoglobulin molecules.

Animals↗
PubMed1977

Cellular mechanisms in the protection against infection by Listeria monocytogenes in mice.

Listeria monocytogenes, in doses of 2-0 X 10(3) to 3-0 X 10(3) viable organisms, was injected into athymic nude mice, irradiated mice and mice treated with reticuloendothelial system-blocking agents. Viable counts on liver and spleen homogenates were made at intervals after infection. In both nude mice (nu/nu) and normal littermates (nu/+) of BALB/c background, the bacteria grew rapidly for 24 h but increased only slowly thereafter, to reach a plateau of about 10(5) per organ at 72 h. In nu/+ mice, the number of viable bacteria began to decrease after 6 to 9 days, with complete elimination by day 12. In nude mice, the number of Listeria remained at a stable level of approximately 10(5) per organ during the observation period of 21 days. In lethally irradiated nu/+ mice, bacteria grew progressively and extensively to reach 10(7) per spleen and 10(9) per liver by 72 h. Bacterial growth during the first 72 h was markedly enhanced by treatment with carbon particles, dextran sulphate 500 or silica. These enhancing effects were also observed in nude mice and in AKR, C3H/He and C57BL/6 animals. We conclude that both non-immune phagocytes and T cell-dependent mechanisms contribute to the resistance of mice to Listeria infection.

Animals↗
PubMed1982

Mechanism of depletion of T lymphocytes from the spleen of mice infected with Listeria monocytogenes.

Marked changes in the splenic lymphocyte populations during murine infection with Listeria monocytogenes were observed histologically and quantitated by the immunofluorescence of Thy-1+ immunoglobulin (Ig-) (T) and Ig+ (B) cells. Cells were depleted from the T-dependent areas of the spleen, and the number of T cells in suspensions prepared from spleens of mice 1 to 3 days after primary or secondary infection were less than 1/10 of normal. High numbers of alcohol-killed Listeria sp. did not cause any depletion. Depletion was not prevented by adrenalectomy. Although injected radiolabeled T cells distributed normally between spleen, liver, lymph node, and gut in infected mice, there appeared to be a barrier to their entry into depleted T-dependent areas of the spleen. Evidence for the destruction of T cells, but not of B cells, in the infected mouse spleen was obtained.

Adrenalectomy↗
PubMed1989

Investigation of an outbreak of listeriosis: new hypotheses for the etiology of epidemic Listeria monocytogenes infections.

From December 1986 to March 1987 an outbreak of Listeria monocytogenes infection occurred in the Philadelphia metropolitan area. A patient-control study showed patients were more likely than controls to have had an ill family member and to have used antidiarrheal medication during the month before their illness. Diet histories showed patients were significantly more likely to have eaten ice cream or salami than were controls, and to have shopped at one grocery store chain. Subtyping of L. monocytogenes isolates of patients showed no predominant strain, and cultures of food products eaten by patients were negative except for Brie cheese eaten by one patient. With no predominant strain of L. monocytogenes in the patients, a common source for this outbreak is unlikely. Thus, the identified risk factors may have been associated with carriage of L. monocytogenes and a coinfecting organism may have precipitated disseminated disease. Possible cofactors should be considered in investigations of future outbreaks of listeriosis.

Adolescent↗
PubMed1988

Listeria monocytogenes infections--therapeutic possibilities and problems.

Listeriosis in humans is a rare disease, which, however, is known to be epidemic and endemic. The prognosis has remained unsatisfactory up to today, the fatality being at least 10% and often considerably higher depending on the clinical features of the disease and the patient's age. Three population groups are at risk: pregnant women, fetuses and newborn infants. Furthermore, immunosuppression in older patients due to disease, therapy, or age also plays a role. The incidence of Listeria infections in patients over 45 is clearly increasing. Due to the nature of the pathogen (in vivo bactericidal concentrations of antibiotics are often not attainable; intracellular growth) a high dosage of ampicillin is recommended. Although the present therapeutic possibilities are not satisfactory, a combination of ampicillin and an aminoglycoside appears to be the best therapy at present. Other combinations such as rifampicin and beta-lactam antibiotics have exhibited in vitro antagonism. The preferred therapy, ampicillin, can only be recommended with reservations because it is not optimally effective.

Adult↗
PubMed2005

Potential antimicrobial effects of human lactoferrin against oral infection with Listeria monocytogenes in mice.

Listeria monocytogenes is a food-borne pathogen that causes serious listeriosis in humans. Antimicrobial effects of human lactoferrin (hLF) against L. monocytogenes have been clearly demonstrated in in vitro studies. However, in vivo studies have not been reported yet. This study investigated whether the oral administration of hLF could inhibit oral infection of listeria in BALB/c mice. The MICs for several strains of L. monocytogenes were determined, and the most sensitive strain was used for the animal work. hLF was administered to BALB/c mice for 7 days, commencing 4 days before oral infection. The effect of hLF was determined by bacterial enumeration and histopathological analysis of the liver and spleen, which are well-known as the major targets of oral listeria infection in mice. In bacterial enumeration, hLF decreased the number of L. monocytogenes cells in the liver. Histopathologically, the size and frequency of necrotic foci in the liver samples decreased with hLF administration. However, these changes were not observed in the spleen samples. The mRNA levels of inflammatory cytokines, such as interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma, decreased in the liver of mice receiving hLF. This study has shown that hLF decreases the hepatic colonization of L. monocytogenes, hepatic necrosis and expression of inflammatory cytokines. It revealed that perorally given hLF could mediate antimicrobial and anti-inflammatory activities remote from the gut (i.e. in the liver) of mice challenged with L. monocytogenes.

Animals↗