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Results for “LISTERIA INFECTIONS”

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PubMed1983

Isolation of a factor from cancer ascitic fluid increasing susceptibility of mice to Listeria infection.

A low-molecular-weight factor (less than 1000) which impairs the capacity of normal mice to resist Listeria infection has been isolated from the ascitic fluid of tumor-bearing mice. The factor showed potent suppressive activity when as little as 0.2 ml of 1:10(5) dilution of the factor was given iv to mice. The factor impaired stage 2 (72 hr after infection) of Listeria elimination in the liver when circulating monocytes migrate from the blood to the liver to begin eliminating the bacteria, but not stage 1 (within 24 hr after infection) when Listeria elimination depends on resident liver macrophages. The factor also inhibited macrophage accumulation in the peritoneum of mice after ip injection of phytohemagglutinin and macrophage chemotaxis in vitro. The factor was heat labile and lost its suppressive activity after being heated at 56 degrees C for 30 min. The factor was detectable in the ascitic fluid rather late after tumor implantation and its production was closely related to tumor growth.

Animals↗

PubMed2006

The effect of centaurein on interferon-gamma expression and Listeria infection in mice.

We previously found that centaurein enhanced IFN-gamma transcription in T cells. Here, we demonstrate that centaurein increased the IFN-gamma expression in T and NK cells and the serum IFN-gamma level in mice. Centaurein elevated the transcription of T-bet but not GATA-3, which is consistent with its effect on that of IFN-gamma but not IL-4. Additionally, centaurein effectively protected mice against Listeria infection. Moreover, centaurein per se or in combination with antibiotics could treat Listeria infection. Our mechanistic studies suggest that centaurein augments IFN-gamma expression via a transcriptional up-regulation of T-bet and that centaurein protects against or treats Listeria infection via a modulation of IFN-gamma expression.

Animals↗

PubMed2003

Effect of lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on the susceptibility to Listeria infection.

We studied the effect of lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the susceptibility to Listeria infection of offspring in C57BL /6NCji mice. The offspring were nursed by TCDD-treated dams and exposed to TCDD from birth to weaning via milk. The exposure had little effect on the weights of immune organs and the spleen or the thymus cell population in the dams and offspring, but it enhanced the production of tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) in the serum after Listeria infection. The clearance of Listeria monocytogenes from the spleen was impaired in the off-spring. These results suggest that the exposure to TCDD of the offspring via milk disrupted the host resistance of the offspring, even though the main immune parameters were unchanged.

Animals↗

PubMed2005

Surveillance of listeria infections in Europe.

In addition to the economic consequences and threats associated with outbreaks, listeriosis remains of great public health concern, as it has one of the highest case fatality rates of all the foodborne infections (20%-30%), and has common source epidemic potential. Changes in the way food is produced, distributed and stored have created the potential for diffuse and widespread outbreaks involving many countries. In 2002, a survey was carried out to assess the need for and the feasibility of a European network on listeria infections in humans. Data on surveillance systems and laboratory methods were collected through two postal surveys sent to the national Centres for communicable disease surveillance and to the listeria reference laboratories. Surveillance systems for listeria infections were in operation in 16 out of the 17 countries surveyed, and 16 countries had a national reference laboratory (NRL). All countries based their case definition of listeriosis on the isolation of Listeria monocytogenes. Fourteen NRLs performed at least one typing method on human strains. At least 13 countries already carried out or expressed willingness to carry out characterisation of isolates by pulsed field gel electrophoresis (PFGE) of L. monocytogenes strains isolated from human cases following a standard protocol. The participants concluded that there was a clear added value to having a European surveillance network for listeria infections, particularly for outbreak detection and investigation, and that a surveillance network based on the existing national surveillance systems was feasible.

Disease Outbreaks↗

PubMed1987

Indomethacin in vivo increases the sensitivity to Listeria infection in mice. A possible role for macrophage thromboxane A2 synthesis.

This paper demonstrates that in the presence of indomethacin, a cyclooxygenase inhibitor, 100% of the mice died when infected with live Listeria, whereas none of the animals died in the absence of the drug. The death of the animals correlated with the numbers of bacteria found extraperitoneally in the spleen and not with the Ia expression of the peritoneal macrophages. Increases in the spleen bacterial numbers between mice treated with either indomethacin or a specific thromboxane synthase inhibitor, OKY1581, and those not receiving either drug, were found as early as 2-4 h after infection. The differences in the initial increased bacterial spleen counts in the presence of indomethacin were reversed by administration of a stable thromboxane A2 analog or another potent vasoconstrictor, phenylephrine. Because thromboxane A2 does not regulate macrophage or T cell functions directly (Tripp, C.S., A. Wyche, E.R. Unanue, and P. Needleman, 1986, J. Immunol., In press; and Ceuppens, J.S., S. Vertessen, H. Deckmyn, and J. Vermylen, 1985, Cell Immunol., 90:458-463), but is probably generated at the site of an infection (Tripp, C.S., K.M. Leahy, and P. Needleman, 1985, J. Clin. Invest., 76:898-901), these data suggest an important role for the vasoconstrictive properties of thromboxane A2 in the regulation of immunity to Listeria infection.

Animals↗

PubMed1991

[Asymptomatic placental Listeria infection].

A case of Listeria monocytogenes placental infection without foetal contamination is reported. The infant, normal at birth, developed progressive and severe neurological involvement. At 8 months of age, magnetic resonance imaging showed a bilateral cerebral atrophy. The responsibility of placental damage in altering the utero-placental blood flow with subsequent foetal hypoxia is discussed.

Acute Disease↗

PubMed2004

CpG oligodeoxynucleotides improve the survival of pregnant and fetal mice following Listeria monocytogenes infection.

Listeria infection during pregnancy can cause the death of both mother and fetus. Previous studies established that immunostimulatory CpG oligodeoxynucleotides (ODN) increase the resistance of healthy adult mice to many infectious pathogens, including Listeria monocytogenes. This study examines whether the innate immune response elicited by CpG ODN can reduce the susceptibility of pregnant mice to lethal listeria challenge. The results indicate that CpG ODN treatment significantly improves maternal survival and reduces pathogen transmission to offspring. CpG ODN administered during pregnancy did not induce abortion, birth defects, or reduce the size or health of litters. These findings suggest that CpG ODN may provide a safe and effective means of improving the health of mothers and fetuses during pregnancy.

Adjuvants, Immunologic↗

PubMed1989

Human tumor necrosis factor increases the resistance against Listeria infection in mice.

The resistance in mice against Listeria infection was augmented by treatment with recombinant human tumor necrosis factor (TNF). To elucidate this phenomenon, we examined the effect of TNF on macrophage activation. TNF-treated macrophages had listericidal activity in vitro and superoxide anion production. In addition, macrophage migration was inhibited in the presence of TNF. Therefore, activation of macrophages by TNF was similar to activation by macrophage-activating factor or macrophage-migration-inhibitory factor.

Animals↗

PubMed1986

Low molecular weight immunosuppressive factors found in elevated amounts in cancer ascitic fluids of mice. 2. 1-Methyladenosine isolated from cancer ascitic fluids enhances Listeria infection in mice.

The low molecular weight fraction (mol wt less than 1,000) of Ehrlich cancer ascitic fluid has been known to enhance Listeria infection in mice. Chemical characterization of the entities in this fraction revealed four purine and pyrimidine analogues, i.e. uric acid, uracil, pseudouridine and 1-methyladenosine (m1Ado). When the effect of each of these components was studied on Listeria infection in mice, only m1Ado markedly enhanced the infection and killed the mice within a short period. The optimal enhancement was obtained when m1Ado was given intravenously to mice 3-6 days before the infection at a concentration of between 1 and 100 micrograms/mouse. On the other hand, uric acid, uracil and pseudouridine failed to show such an enhancing effect. m1Ado inhibited macrophage accumulation in the peritoneal cavity of mice after an intraperitoneal injection of phytohemagglutinin. Although m1Ado did not show any inhibitory effect on the phagocytic and bactericidal activities of macrophages in vitro, peritoneal macrophages obtained from mice which received m1Ado 3 days ahead revealed impaired bactericidal activity, suggesting the migration of different cell populations from the bone marrow of m1Ado-receiving mice. The results may suggest that m1Ado is a major factor in tumor ascites causing, in small doses, an impairment of macrophage functioning as can be detected in tumor-bearing hosts.

Adenosine↗

PubMed2002

T-cell activation, proliferation and apoptosis in primary Listeria monocytogenes infection.

Listeria monocytogenes infection of mice leads to a rapid expansion of activated T cells, followed by a decline in specific cells once the bacteria are eliminated. In order to define the relationship between T-cell proliferation and activation, and to investigate the role of apoptosis in limiting the expansion, the expression of activation markers, uptake of 5-bromo-2'-deoxyuridine (BrdU) in vivo and the incidence of apoptosis was investigated. Increased numbers of T cells expressing the activated phenotype CD25+, CD44hi and CD62Llo were detected 4 days after infection. Expression of CD25 (IL-2Ralpha chain) on CD4+ and CD8+ T cells peaked at this time and returned to normal by day 7. In contrast, CD44hi and CD62Llo persisted, with the maximum proportion occurring at 7 days after infection. This was accompanied by a burst of in vivo proliferation of CD4+ and CD8+ T cells occurring between day 5 and 7. Apoptosis, which is presumably needed to control this expansion of T cells, also peaked at 7 days after infection. Apoptosis occurred preferentially amongst T cells which had proliferated. Most but not all proliferating T cells had down-regulated their CD62L marker. While most apoptotic T cells were CD62Llo, again not all had down-regulated this marker. Hence, CD25 expression peaked early, but expression of other activation markers, in vivo proliferation and apoptosis coincided after Listeria infection. T cells that had proliferated were over-represented in the apoptotic population.

Animals↗

PubMed1985

Killed Listeria-induced suppressor T cells involved in suppression of delayed-type hypersensitivity and protection against Listeria infection.

Pretreatment of mice by intravenous injection with killed Listeria provided neither delayed-type hypersensitivity to Listeria protoplasm nor protection against Listeria infection. Assuming that this suppression is due to suppressor cells, we attempted to clarify their induction and characterization. Pretreatment with killed BCG instead of killed Listeria suppressed the induction of DTH and protection in subsequent Listeria-immunized mice. Conversely, pretreatment with killed Listeria suppressed subsequent induction of DTH to PPD or protection from tuberculosis. Thus, these suppressions were induced antigen nonspecifically. Transfer of splenic non-adherent cells from killed Listeria-injected mice which had been treated with anti-BA theta serum plus complement, or had been passed through Sephadex G-10 columns, resulted in both afferent and efferent DTH suppression, suggesting that the DTH suppression is closely associated with suppressor T cells. Moreover, the splenic nonadherent cells from killed Listeria-injected mice showed suppression in vitro of listericidal activity of PEC from Listeria-immune mice in the presence of Listeria protoplasm.

Animals↗

PubMed1980

In vitro proliferation of T lymphocytes from Listeria-infected rodents: assay conditions for rat peritoneal exudate cells and characterization of an inhibitor.

Conditions favorable to [(3)H]thymidine incorporation into antigen-stimulated T lymphocytes from Listeria-infected rats have been established. In cultures of peritoneal exudate (T) lymphocytes purified twice with nylon-wool vigorous antigen-specific proliferation was observed within 2 days. Cultures of lymphocytes from nodes draining a subcutaneous Listeria-infection site differed in that back-ground proliferation was higher than for peritoneal exudate lymphocytes, and [(3)H]thymidine incorporation was maximal at day 3. A critical factor for the rate of proliferation was the lymphocyte-to-macrophage ratio; optimal cultures of peritoneal exudate lymphocytes contained 2 to 5% macrophages. Macrophages exceeding a proportion of 10% strongly, if not completely, inhibited [(3)H]thymidine incorporation into antigen-stimulated lymphocytes. Inhibition was associated with mononuclear cells, adherent to plastic or nylon-wool, of the stimulated or unstimulated peritoneal cavity. It was neither attributable to release of cold thymidine from macrophages nor to rapid degradation of particulate antigen by macrophages. The degree of inhibition reflected the metabolic activity of macrophages; on a cell-for-cell basis, heat-killed and glutaraldehyde-fixed macrophages were less inhibitory, and stimulated macrophages were more inhibitory than macrophages from the unstimulated peritoneal cavity.

Animals↗

PubMed1974

Morphological changes induced by dextran sulfate 500 in mononuclear phagocytes of listeria-infected mice.

Morphological changes involving mononuclear phagocytes in Listeria-infected mice after treatment with dextran sulfate 500 were investigated. Mononuclear phagocytes in livers and spleens, both circulating monocytes and fixed macrophages, showed uptake of electron-dense material. Mononuclear phagocyte changes were most pronounced within granulomatous lesions, where many phagocytes showed large membrane-bound inclusions and extensive cellular damage. It is concluded that dextran sulfate 500 selectively damages mononuclear phagocytes and that, in listerial infection, dextran sulfate 500 renders mononuclear phagocytes unable to express cellular resistance.

Journal Article↗

PubMed1979

[Listeria infection of a twin pregnancy (author's transl)].

A Listeria infection of a twin pregnancy had induced a partus immaturus at 23 weeks. One foetus died in utero of a widespread foeto-placental granulomatosis, while the other one, dying sub-partu, showed only retroplacental abcesses. The unequal extent of the infection in the two placentas -- of diamniotic, dichorionic type -- is interpreted as different stages of the same disease; it could be due to a different resistance to the germ between the two dizygotic foetuses.

Adult↗

PubMed2001

Addition of Maitake D-fraction reduces the effective dosage of vancomycin for the treatment of Listeria-infected mice.

Maitake D-fraction, beta1,6-glucan having beta1,3-branches, has been reported to activate the immune system of the host. To elucidate whether the D-fraction can reduce the clinical effective dosage of antibiotics in the treatment of opportunistic bacterial infection, we examined the effects of D-fraction on the treatment of Listeria monocytogenes-infected mice in combination with vancomycine (VCM), the only antibiotic used for methicillin-resistant Staphylococcus aureus (MRSA). Listeria-infection was introduced by its inoculation into the abdominal cavity of mice. Without treatment, all inoculated mice died within 3 days after the inoculation. In contrast, in the mice treated with combined therapy of D-faction (10 mg/kg per day) and VCM (10 mg/kg per day), the survival rate was maintained at 60% on the 10th day after the inoculation, which was superior to that of mice treated with VCM alone (10 mg/kg per day). To investigate the mechanism underlying the reinforcement of VCM treatment by the D-fraction, the activities of macrophages and splenic T cells of Listeria-infected mice were evaluated. In mice administered with both D-fraction and VCM, macrophages produced 2.7 times as much interleukin-1 as that of non-treated control mice. The bactericidal activity of splenic T cells was also enhanced by 2.6 times of that of non-treated control mice. These results indicate that D-fraction activates immuno-competent cells, induced cytokine production, and consequently enhanced the bactericidal activities of the splenic T cells against Listeria monocytogenes, suggesting the clinical benefit of D-fraction in the case of anti-bacterial treatment for patients with high risks.

Abdomen↗

PubMed1978

Listeria infection in transplant patients. Five cases and a review of the literature.

We report five cases of Listeria monocytogenes infection in renal transplant patients at the University of Minnesota and compare them to 15 additional patients reported on in the United States literature. All patients were noted to have fever, malaise, and nonspecific symptoms of infection. There were no consistent diagnostic laboratory findings except for positive bacteriologic studies. Successful treatment consisted of intravenous penicillin G potassium in most cases (ampicillin sodium was required in two patients). Mortality was low, with only one patient of the 20 (and no Minnesota patients) dying of listeriosis. The time interval from transplant to infection was definitively longer in the Minnesota patients; this may be due to the routine use of sulfisoxazole following renal transplantation. Listeria infection, though mild itself, may herald other infectious processes in the immunoincompetent host.

Adolescent↗

PubMedDate not supplied

Resistance of gnotobiotic nude mice to Listeria infection.

Unlike the acute and short-term course of experimental listeriosis in phenotypically normal (nu/+) mice, Listeria monocytogenes infection in conventionally raised athymic Nude mice results in chronic inflammation with persistence of bacteria and lesions in the internal organs such as liver and spleen. Although it could be shown that germfree Nude mice had no intestinal microbial flora and lacked measurable serum immunoglobulins, neither the course nor the histomorphology of experimental listeriosis differed significantly from that of their conventionally raised littermates. The results indicate that the typical response of Nude mice to Listeria infection is primarily determined by inborn factors and not by prior antigenic stimulation.

Animals↗

PubMed2003

Suppression of cell-mediated immune responses to listeria infection by repeated exposure to diesel exhaust particles in brown Norway rats.

Diesel exhaust particles (DEP) have been shown to alter pulmonary immune responses to bacterial infection. Exposure of rats to 100 mg/m(3) DEP for 4 h was found to aggravate Listeria monocytogenes(Listeria) infection at 3 days postinfection, but the bacteria were largely cleared at 7 days postinfection due to the development of a strong T cell-mediated immunity. In the present study, we examined the effects of repeated DEP exposure at lower doses on pulmonary responses to bacterial infection. Brown Norway rats were exposed to DEP by inhalation at 20.62 +/- 1.31 mg/m 3 for 4 h/day for 5 days, followed by intratracheal inoculation with 100,000 Listeria at 2 h after the last DEP exposure. DEP-exposed rats showed a significant increase in lung bacterial load at both 3 and 7 days postinfection. The repeated DEP exposure was shown to suppress both the innate, orchestrated by alveolar macrophages (AM), and T cell-mediated responses to Listeria. DEP inhibited AM production of interleukin- (IL-) 1beta, tumor necrosis factor- (TNF-) alpha, and IL-12 but enhanced Listeria-induced AM production of IL-10, which has been shown to prolong the survival of intracellular pathogens such as Listeria. DEP exposure also suppressed the development of bacteria-specific lymphocytes from lung-draining lymph nodes, as indicated by the decreased numbers of T lymphocytes and their CD4(+) and CD8(+) subsets. Furthermore, the DEP exposure markedly inhibited the Listeria-induced lymphocyte secretion of IL-2 at day 7, IL-10 at days 3 and 7, and interferon- (IFN-) gamma at days 3 to 10 postinfection when compared to air-exposed controls. These results show a sustained pattern of downregulation of T cell-mediated immune responses by repeated low-dose DEP exposure, which is different from the results of a single high-dose exposure where the acute effect of DEP aggravated bacteria infection but triggered a strong T cell-mediated immunity.

Air Pollutants↗