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PubMed1981

Bacillus Calmette-Guérin (BCG) decreases resistance to Listeria monocytogenes infection in mice.

Bacillus Calmette-Guérin (BCG) inoculation has been shown to inhibit certain immune functions. To determine whether this inhibition adversely affects host defences against infection, the effect of BCG on Listeria infection in mice was investigated. Mice were injected intravenously (i.v.) with Listeria monocytogenes and 24-96 hr later were inoculated with 8 x 10(6) BCG. Mice given BCG and Listeria had a greater mortality and higher spleen Listeria counts than mice given Listeria alone. An increased number of bacteria in spleens was noted as early as 24 hr after BCG inoculation. Peritoneal macrophages from mice receiving both organisms had a decreased capacity to kill Listeria in vitro. In addition, BCG inoculation suppressed delayed hypersensitivity responses and in vitro spleen cell proliferative responses to Listeria antigen. Suppression of spleen cell proliferative responses was associated with an adherent, non-T lymphocyte subpopulation. The data indicate that BCG administration decreases resistance to intracellular pathogens by abrogating normal cellular defences.

Animals↗

PubMed1988

Increased prostaglandin E release and tumor cytostasis by resident Kupffer cells during Listeria monocytogenes infection.

Liver macrophages isolated from Listeria monocytogenes-infected mice were studied for their functional capacities in vitro. Spontaneous release of prostaglandin E and tumor cytostatic activity by liver macrophages of infected mice were markedly enhanced when compared to controls. Irradiated mice showing no increase in the number of their liver macrophages after Listeria monocytogenes infection, in contrast to solely infected mice, nevertheless demonstrated comparable activities. Our data suggest that radioresistant liver macrophages, most probably resident Kupffer cells, can be activated during in vivo infection to express enhanced effector functions.

Animals↗

PubMed1992

Deferoxamine increases the susceptibility of beta-thalassemic, iron-overloaded mice to infection with Listeria monocytogenes.

The effect of the iron chelator deferoxamine (DFO) on resistance to infection with Listeria monocytogenes in mice with a condition analogous to human beta-thalassemia was studied. Intraperitoneal injection of 10 mg DFO resulted in significantly increased mortality when given one, three and six days before infection with L. monocytogenes (for all three time points, p less than 0.02). There were no significant differences in hematocrit, plasma iron, or splenic iron content between the two groups of mice during these time periods. In addition, splenic counts of L. monocytogenes were not significantly higher in DFO-treated compared to saline-treated mice three days after infection. Moreover, background C57Bl/6J mice were not more susceptible to Listeria infection after receiving DFO than were saline-treated controls. In conclusion, acute administration of DFO increases the susceptibility of beta-thalassemic mice to L. monocytogenes. The effect is not seen in background mice and suggests that DFO increases susceptibility to Listeria infection only in animals with iron overload.

Animals↗

PubMed1999

Infrarenal endoluminal bifurcated stent graft infected with Listeria monocytogenes.

Prosthetic graft infection as a result of Listeria monocytogenes is an extremely rare event that recently occurred in a 77-year-old man who underwent endoluminal stent grafting for infrarenal abdominal aortic aneurysm. The infected aortic endoluminal prosthesis was removed by means of en bloc resection of the aneurysm and contained endograft with in situ aortoiliac reconstruction. At the 10-month follow-up examination, the patient was well and had no signs of infection.

Aged↗

PubMed1991

Effects of macrophage colony-stimulating factor on reduction of viable bacteria and survival of mice during Listeria monocytogenes infection: characteristics of monocyte subpopulations.

Mice could well tolerate infection with a lethal dose of Listeria monocytogenes after intraperitoneal preinjections with 250 micrograms of macrophage colony-stimulating factor (M-CSF) per kg of body weight for 5 days. The characteristic changes in the surface markers (Mac-1, LFA-1, and F4/80) of peripheral monocytes were also investigated in order to analyze the mechanism of protection by M-CSF. This investigation shows the excellent effect of intraperitoneal preinjections of M-CSF on the reduction of viable Listeria organisms and the improvement of survival after an intravenous Listeria infection.

Animals↗

PubMed1998

Early IFN-gamma production and innate immunity during Listeria monocytogenes infection in the absence of NK cells.

NK cells are believed to play a mandatory role during the early phases of Listeria monocytogenes infection by producing IFN-gamma, which is required for the activation of macrophage effector functions. Mice deficient in the common cytokine receptor gamma-chain (gamma(c)-/-), which completely lack NK cells, were used to examine whether NK cells were essential for resistance to Listeria infection in vivo. Surprisingly, infected gamma(c)-/- mice showed normal innate immunity and macrophage responses against sublethal Listeria infection 2 days postinfection. At this time point, gamma(c)-/- mice showed increased blood IFN-gamma levels compared with those in noninfected controls, demonstrating an NK-independent source of IFN-gamma, which explains early resistance. Listeria-infected gamma(c)-/- x recombinase-activating gene-2-/- double-deficient mice were unable to produce IFN-gamma and were highly susceptible to L. monocytogenes. Since T cells, but not B cells, are major IFN-gamma producers, and gamma(c)-/- T cells were found to be efficient IFN-gamma producers in vitro, we conclude from these results that T cells functionally replace NK cells for the early IFN-gamma production that is necessary for activating the innate immune system following infection with L. monocytogenes. This novel observation in listeriosis underscores how the adaptive immune response can maintain and influence innate immunity.

Animals↗

PubMed1977

Bacteriological and histopathological evaluation of guinea pigs after infection with Listeria monocytogenes.

Randomly bred guinea pigs were infected with Listeria monocytogenes using the intracardial, intravenous and intraperitoneal routes of infection. Doses of Listeria ranged from 5 to 1,000 x the 50% lethal dose based on the 50% lethal dose for intracardially injected Listeria. A complete necropsy was performed on all animals that died after infection. Gross and microscopic examination of tissues revealed major pathological features which include myocarditis, edema and congestion with interstitial pneumonitis present in the lungs, and fatty hepatic changes with focal necrosis. For all or a majority of the animals, large numbers of Listeria were likewise recovered from these organs and from lymph nodes, spleen, kidneys, and adrenal gland tissue. Of the three routes of infection used, guinea pigs were most susceptible to Listeria injected via the intracardial route. The relatively high lethal dose of listeric for the quinea pig, however, suggests that the organism is a low-grade pathogen for this species.

Animals↗

PubMedDate not supplied

Treatment of Listeria monocytogenes infection with trimethoprim-sulfamethoxazole: case report and review of the literature.

A 55-year-old female recipient of an orthotopic liver transplant, who was receiving azathioprine, prednisone and cyclosporin, developed bacteremia due to Listeria monocytogenes. Because of a penicillin allergy, the patient was treated primarIly with trimethoprim-sulfamethoxazole, to which she responded well. The prior literature on use of trimethoprim-sulfamethoxazole in listeria infections is reviewed, and future recommendations are considered. On the basis of the experience described in this case report as well as a review of the literature, trimethoprim-sulfamethoxazole appears to be an effective treatment of listeria infections.

Drug Combinations↗

PubMed2006

[Listeria meningitis in a patient with Crohn's disease--a seldom, but clinically relevant adverse event of therapy with infliximab].

A 42-year-old man with steroid-dependent Crohn's disease developed fever, vomiting and headache after the second administration of infliximab. Extensive microbiological and biochemical work-up revealed an atypical meningitis caused by Listeria monocytogenes. After antibiotic therapy of 21 days duration, the patient could be discharged from hospital totally recovered without any further complications. As previously demonstrated, TNF-alpha plays an important role in resistance to Listeria monocytogenes. Listeria infections have been reported in 26 patients receiving TNF-alpha inhibitors. An additional therapy with other immunosuppressants increases the risk for Listeria infections. Listeria meningitis is a seldom adverse event of therapy with TNF-alpha inhibitors but is associated with a high lethality. Therefore patients should be informed about the possible adverse event of a Listeria infection during anti-TNF-alpha therapy before receiving immunosuppressive treatment. Furthermore, therapy with TNF-alpha inhibitors should only be executed within a close doctor-patient relationship and in cooperation with specialised centres.

Adult↗

PubMed1996

Influence of beta 2-microglobulin expression on gamma interferon secretion and target cell lysis by intraepithelial lymphocytes during intestinal Listeria monocytogenes infection.

Numerous microbial pathogens, including Listeria monocytogenes, enter the host through the intestine. Although relatively little is known about the biological functions of intestinal intraepithelial lymphocytes (i-IEL), they are generally considered a first line of defense against intestinal infections. In the mouse, the vast majority of i-IEL express the CD8 coreceptor either as a CD8 alpha/alpha homodimer or as a CD8 alpha/beta heterodimer. The CD8 receptor of T-cell receptor TcR gamma/delta i-IEL is exclusively homodimeric, whereas the CD8-expressing TcR alpha/beta i-IEL segregate into equal fractions of CD8 alpha/alpha and CD8 alpha/beta cells. We infected beta 2-microglobulin (beta 2m)+/- mice (possessing all i-IEL populations) and beta 2m -/- mutant mice (lacking all CD8 alpha/beta + i-IEL and having few CD8 alpha/alpha + TcR alpha/beta i-IEL) with L. monocytogenes per os and determined their biological functions after TcR ligation with monoclonal antibodies. Cytolytic activities of TcR alpha/beta and TcR gamma/delta i-IEL from beta 2m +/- mice were not influenced by intestinal listeriosis. Cytolytic activities of TcR alpha/beta i-IEL were impaired in uninfected beta 2m -/- mice, but this reduction was reestablished as a consequence of intestinal listeriosis. Frequencies of gamma interferon (IFN-gamma)-producing TcR alpha/beta i-IEL in uninfected beta 2m -/- mice were reduced, compared with that in their heterozygous controls. Equally low frequencies of IFN-gamma-producing TcR gamma/delta i-IEL in beta 2M +/- and beta 2m-/- mutants were found. Listeriosis increased frequencies of INF-gamma-producing TcR alpha/beta and TcR gamma/delta i-IEL in both mouse strains. Most remarkably, the proportion of IFN-gamma-producing TcR gamma/delta i-IEL was elevated 10-fold in listeria-infected beta 2M -/- mice. Our findings show that the beta 2m-independent CD8 beta- i-IEL expressing either TcR alpha/beta or TcR gamma/delta are stimulated by intestinal listeriosis independent of regional beta 2m expression. We conclude that the three major CD8+ i-IEL populations are stimulated by intestinal listeriosis and that CD8 beta- i-IEL compensate for the total lack of CD8 beta+ i-IEL in beta 2M -/- mutant mice. Hence, in contrast to the peripheral immune system, which crucially depends on CD8 alpha/beta + TcR alpha/beta lymphocytes, the mucosal immune system can rely on additional lymphocytes expressing the CD8 alpha/alpha homodimer.

Animals↗

PubMed1995

Listeria monocytogenes infection in a patient treated with methotrexate for rheumatoid arthritis.

We describe a patient with rheumatoid arthritis who developed bacteremia from Listeria monocytogenes after treatment with low dose oral pulse methotrexate. We discuss possible immunologic mechanisms for susceptibility to Listeria infections. As the elderly population increases with more frequent use of immunosuppressive medications, clinical suspicion must be maintained to correctly diagnose and treat infections such as Listeria.

Aged↗

PubMed1978

Listeria pneumonitis: induction of immunity after airborne infection with Listeria monocytogenes.

After implantation of approximately 10(3) Listeria monocytogenes organisms into the lungs, mice develop an acute pneumonitis with dissemination of infection to a mediastinal lymph node (MedLN), liver, and spleen. The infections in a MedLN and spleen resolve in approximately 7 days, but the lung infection persists for a few days longer. Pneumonitis is accompanied by a lymphoproliferative response in a MedLN and spleen, and immunity to Listeria is conferred adoptively with MedLN and spleen cells but not with mesenteric lymph node cells. Although the spleen appears to be the major repository of sensitized lymphocytes, splenectomized mice combat Listeria pneumonitis as effectively as normal mice. It is concluded that the induction of immunity to lung infection with L. monocytogenes is efficient and that the cause for the rather protracted pneumonitis is due to a defect in the expression of the cell-mediated immunity effector mechanism.

Animals↗

PubMedDate not supplied

[The role of nitric oxide in Listeria encephalitis of ruminants and in rats intracisternally infected with Listeria monocytogenes].

Listeria monocytogenes is a Gram-positive facultative intracellular bacteria which infects a wide range of hosts. In ruminants, infection with L. monocytogenes frequently causes encephalitis, which is usually fatal in sheep and goat, while cattle often recover with antibiotic therapy. Since the role of NO in the control of Listeria is controversial, we have studied the expression of iNOS in the brains of cattle, sheep and goats which had succumbed to listeria encephalitis. iNOS was demonstrated in decreasing intensity in the M phi of microabscesses from cattle, sheep and goat. iNOS expression was accompanied by NT in the microabscesses of cattle, but was only present to a low degree in sheep and was absent in goats. This is indirect evidence for differences in the ability to produce NO in the three species. Presence of iNOS and NT were inversely correlated with the numbers of bacteria. While microabscesses of goats contained high amounts of L. monocytogenes they occurred only rarely in cattle. To corroborate our hypothesis that NO is involved in the control of listeria encephalitis a new animal model was developed. Eleven day old infant rats were infected intracisternally with a low dose of L. monocytogenes. This resulted in a transient meningoencephalitis with moderate clinical signs and low mortality. Listeria proliferated strongly in the inflammatory lesions during the first days of infection, reached a peak at day 4 and were eliminated until day 7. The presence of bacteria was closely accompanied by high numbers of iNOS-expressing M phi and the formation of NT. Administration of the iNOS inhibitor L-NIL or the radical scavenger PBN resulted in rapid death of the treated animals. However, the increase in bacterial numbers was one order of magnitude higher for animals treated with PBN compared with L-NIL administration. This shows that NO plays an important role in the control of a brain infection with Listeria, but suggests that reactive oxidants other than NO are also involved. In conclusion, our findings point to a possible involvement of the differences in the ability to express iNOS and subsequent NO production in the different clinical outcome of listeria encephalitis in cattle and small ruminants.

Animals↗

PubMed1998

Nitric oxide mediates immunosuppression induced by Listeria monocytogenes infection: quantitative studies.

Our laboratory has shown that immunization of mice with an attenuated strain of Salmonella typhimuriuminduces profound suppression in the capacity of splenocytes to mount an in vitro antibody plaque-forming cell (PFC) response to sheep red blood cells (SRBC) and to proliferate in response to mitogens. In vitro addition of NG-monomethyl-L-arginine (NMMA), an inhibitor of nitric oxide (NO) synthase, to cell cultures from Salmonella-immunized mice completely blocked suppression of the PFC responses, implicating that NO is the suppressor factor. The present study quantified the role of nitric oxide in immunosuppression induced by Listeria monocytogenes, a gram positive intracellular pathogen of macrophages. Listeria infection resulted in suppression of the PFC assay at inoculating doses of greater than 6.5x10(3)colony forming units, with no suppression observed at lower doses. Suppression correlated with increased nitrite production. Addition of NMMA to spleen cell cultures taken from Listeria-infected mice completely blocked suppression of the PFC response, and returned nitrite production to baseline levels. In regard to Listeria-induced suppression of responses to the mitogen, Concanavalin A (Con A), the parameters were different from those observed for the PFC response. There was a direct correlation between the log10of the inoculating dose of Listeria and degree of immunosuppression, with suppression observed at doses as low as 1x10(3)cells. Addition of NMMA to the Con A-stimulated cultures resulted in reduced nitrite levels, but only partial restoration of the proliferative responses. Co-culture of splenocytes from Listeria inoculated mice with normal splenocytes in media with NMMA and reduced levels of L-arginine resulted in complete reversal of suppressed responses to Con A. Similar differences in ease of reversing suppression of the PFC response, as compared with responses to Con A, were previously noted using cells taken from Salmonella-infected mice. The present results show that a gram positive intracellular pathogen of macrophages, L. monocytogenes, induces immunosuppression in mouse spleen cells by a nitric oxide mediated mechanism that closely parallels that induced by the gram negative pathogen, S. typhimurium.

Animals↗

PubMed1995

CD8 T lymphocytes specific for the secreted p60 antigen protect against Listeria monocytogenes infection.

The ability of Listeria monocytogenes to gain access to the cytoplasm of infected cells results in the processing and presentation of bacterial Ags through the MHC class I pathway. As a result, CD8 T cells are the most effective mediators of acquired immunity in the mouse model of L. monocytogenes infection. CD8 T cells specific for a single nonamer epitope derived from the secreted virulence factor listeriolysin O (LLO) can protect H-2d mice against lethal infection. Bacteria lacking LLO are avirulent and do not elicit protective immunity in mice. Thus, the failure of LLO minus L. monocytogenes to elicit protective immunity could be caused either by their inability to enter the cytoplasm or to the lack of LLO-derived peptide epitopes. In this report we provide evidence that H-2d restricted CD8 T cells with specificity for another L. monocytogenes protein, the secreted p60 molecule, can protect against infection. Our studies further demonstrate that LLO-dependent induction of protective immunity results from access of the bacterium to the cytoplasm. In addition, these studies provide support for the hypothesis that secreted bacterial proteins are the most important targets for protective CD8 T cell-mediated immunity.

Animals↗

PubMed1966

Mechanisms of pathogenesis in Listeria monocytogenes infection. I. Influence of iron.

Sword, C. P. (The University of Kansas, Lawrence). Mechanisms of pathogenesis in Listeria monocytogenes infection. I. Influence of iron. J. Bacteriol. 92: 536-542. 1966.-The effects of ferric and ferrous iron as well as other cations on Listeria infection in mice were studied. Iron compounds caused a reduction in the ld(50) dose of Listeria, and, when added to a synthetic medium, proved stimulatory for in vitro growth of the organism. Bacterial counts on spleen and liver tissue from iron-treated mice showed that iron injections caused more rapid growth of bacteria and resulted in higher numbers of organisms in the tissue. The reticuloendothelial system did not appear to be impaired by this treatment. Immunized animals were not affected by iron treatment during challenge. Mice with experimentally induced hemolytic anemia showed increased susceptibility to listeriosis, whereas those treated with Desferal, a specific iron-chelating agent, appeared more resistant. Iron proved stimulatory for the avirulent strain, 9037-7, and resulted in an ld(50) of 1.3 x 10(4) organisms in iron-treated animals. Growth of L. monocytogenes and mortality from experimental infection appeared to be correlated with availability of iron to the bacteria. The results suggest that host iron metabolism may play a part in the onset and progress of Listeria infections.

Anemia, Hemolytic↗

PubMed1986

An outbreak of type 4b Listeria monocytogenes infection involving patients from eight Boston hospitals.

During September and October 1979, 23 patients admitted to hospitals in the Boston area had systemic Listeria monocytogenes infection. Twenty (87%) of these isolates were L monocytogenes type 4b, whereas only nine (33%) of the isolates serotyped during the preceding 26 months had been 4b. Patients with type 4b Listeria infection during the epidemic period (case patients) differed from patients with sporadic Listeria infection in the preceding two years in that more of the case patients had hospital-acquired infection (15/20 vs 4/18), had received antacids or cimetidine before the onset of listeriosis (12/20 vs 3/18), and had gastrointestinal tract symptoms that began at the same time as fever (17/20 vs 4/18). In addition, more case patients took antacids or cimetidine compared with patients matched for age, sex, and date of hospitalization (12/20 vs 10/40). Three foods were preferred by case patients more frequently than by control patients: tuna fish, chicken salad, and cheese. However, the only common feature appeared to be the serving of these foods with raw celery, tomatoes, and lettuce. The raw vegetables may have been contaminated with Listeria, which was able to survive ingestion because of gastric acid neutralization and subsequently to cause enteritis, bacteremia, and meningitis in susceptible hosts. However, we cannot exclude pasteurized milk as a source of this outbreak.

Aged↗

PubMed1999

Xenobiotic-metabolizing enzymes in carp (Cyprinus carpio) liver, spleen, and head kidney following experimental Listeria monocytogenes infection.

Infection of carp with Listeria monocytogenes 4b resulted in decreased liver, spleen, and head kidney enzyme activities, involved in the metabolism of xenobiotics. After infection, cytochrome P-450 levels and ethoxyresorufin O-deethylase (EROD) activity were decreased while conjugation enzymes remained unaffected. The maximum decrease for phase I enzymes occurred on d 3. This loss of monooxygenase levels and activity could not be directly correlated with an increase in the number of organisms, as consistently high bacterial counts were observed in all three organs during infection. The effect of L. monocytogenes infection was also measured in carp exposed to 3-methylcholanthrene (MCA). Cytochrome P-450 levels and EROD activity were significantly reduced, especially on d 3. A significant decreased activity of conjugation enzymes such as glutathione S-transferase (GST) and UDP-glucuronosyltransferase (UDPGT) was also observed for all days studied. Listeria infection inhibited MCA-induced increases in xenobiotic-metabolizing enzyme activities. These results indicate that infection may have deleterious effects on basal cytochrome P-450 monooxygenase levels. Furthermore, MCA treatment aggravates the insult to xenobiotic biotransformation enzymes by L. monocytogenes infection, by impairing a number of detoxification enzymes. These findings could result in significant changes in the susceptibility of fish to pollutants.

Animals↗