[Specific and nonspecific induction of resistance to Listeria infection and hypersensitivity to Listeria factor Ei (author's transl)].
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Animals↗
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Mechanisms of Listeria monocytogenes-mediated modulation of tumor growth.
Studies using Listeria monocytogenes as an antitumor agent were initiated to determine the requirements for Listeria-mediated tumor inhibition to occur. When Strain 13 guinea pigs were injected with an admixture of viable Listeria and a methylcholanthrene-induced fibrosarcoma in a ratio of 1 bacterium to 100 tumor cells, Listeria had a marked capacity to inhibit tumor growth. This confirms an earlier study in our laboratory (M. M. Dustoor, A. Fulton, W. Croft, and A. A. Blazkovec, Infect. Immun. 23:54-60, 1979). At no time did animals exhibit overt symptoms of disease as a result of Listeria infection. Animals treated with antilymphocyte serum, which had previously been shown to abrogate T-cell functions, were no longer able to suppress Listeria-tumor cell mixtures. Treatment in vivo with carrageenan, a macrophage-inhibitory agent, also abrogated Listeria-mediated tumor inhibition. These results suggest that Listeria-mediated inhibition requires intact T-lymphocyte and macrophage function. Experiments in which Listeria was given in admixture with the tumor cells or in the opposite flank demonstrated that the antitumor effects require intimate association of the Listeria and tumor cells. Histopathological studies, showing that macrophages and lymphocytes are the predominant inflammatory cells present at sites of tumor destruction, further suggest a role for these cells in Listeria-mediated inhibition. Animals which had rejected prior Listeria-tumor cell inocula were resistant to rechallenge with the homologous tumor for more than 1 year. This work thus confirms in vitro studies demonstrating that both lymphocytes and macrophages are required for Listeria-mediated tumor inhibition to occur. This study demonstrates that viable Listeria can have potent antitumor effects without causing overt disease as a result of Listeria infection.
Animals↗
Listeria monocytogenes cell walls induce decreased resistance to infection.
A significant decrease in murine resistance to Listeria monocytogenes was induced by using crude Listeria cell wall fraction (LCWF) and purified Listeria cell walls (PF). When equal amounts of these materials were injected, PF was more effective than LCWF in decreasing resistance. The PF effect was dose dependent when measured either as a decrease in 50% lethal dose of the Listeria challenge or as a decrease in survival time of the infected mice. PF apparently does not act directly on the Listeria since it (i) did not cause a change in in vitro growth of Listeria and (ii) did not increase the virulence of Listeria passaged in vivo or in vitro. The greatest decrease in resistance was observed when both PF and the Listeria challenge were injected intraperitoneally, which may suggest a localized effect. A decrease in resistance was seen when PF was given as early as 3 days before challenge. There was little or no decrease in resistance when PF was given 2 days after the Listeria challenge. Mice previously immunized with live Listeria were immune to Listeria challenge. However, after PF injection the immune mice showed a decreased resistance which was of the same order of magnitude as that seen in unimmunized mice. The effect of PF seems to be at least partially nonspecific, since a decrease in resistance to Salmonella typhimurium could also be demonstrated in PF-treated mice. Phagocytosis of Listeria both in vivo and in vitro did not appear to be inhibited by PF, although the ability of PF-treated mice to kill Listeria in the peritoneal cavity was inhibited.
Animals↗
Proposal to validate Listeria swaminathanii sp. nov. and reassign the type strain to UTK S2-0008.
Listeria swaminathanii UTK S2-0008, isolated from soil collected in the Nantahala National Forest in North Carolina, USA, is the only L. swaminathanii strain eligible to serve as the type strain, which is needed to achieve valid status. The previously effectively published type, L. swaminathanii FSL L7-0020T, and previously described strains UTK C1-0015 and UTK C1-0024 do not conform to the International Code of Nomenclature of Prokaryotes' rules for type strains. Additionally, the currently designated type strain (FSL L7-0020T = ATCC TSD-239T) is an atypical representative of L. swaminathanii as it is the only strain lacking catalase activity. Therefore, it is proposed to reassign the type to L. swaminathanii (UTK S2-0008T = CCUG 77280T = LMG 33255T). Whole-genome sequence-based average nucleotide identity (ANI) showed that this strain clustered with the three previously described L. swaminathanii strains (FSL L7-0020 = ATCC TSD-239, UTK C1-0015, and UTK C1-0024; pairwise ANI ranged from 98.71% to 98.83%). All four strains, including the one described here, could not be classified as any validly published Listeria species and showed the highest similarity to Listeria marthii (maximum ANI of 93.92%, in silico DNA-DNA hybridization of 56.2%). L. swaminathanii exhibits the phenotypic characteristics that are currently expected of the Listeria sensu stricto species. This species lacks phenotypic characteristics associated with Listeria pathogenicity (non-hemolytic and negative for phosphatidylinositol-specific phospholipase C activity); the genomes lack genes associated with virulence (all genes found on the Listeria pathogenicity island 1 [LIPI-1], as well as the internalin genes inlA and inlB), which support L. swaminathanii is nonpathogenic.IMPORTANCEThe genus Listeria includes species of significant relevance to food safety, environmental microbiology, and public health. Accurate species identification is critical because misidentification of nonpathogenic species as pathogenic ones can lead to unnecessary recalls and regulatory complications. The validation of Listeria swaminathanii sp. nov. will ensure that this species is formally recognized and has a type strain (UTK S2-0008T) that is representative of the species. This work strengthens diagnostic accuracy by enabling the inclusion of this species in reference databases and inclusivity studies, reducing the risk of false identification. Furthermore, the identification and characterization of Listeria swaminathanii sp. nov. expands our understanding of the genetic and ecological diversity within the genus Listeria, particularly among soil-dwelling strains.
Listeria↗
Macrophage-T cell interactions involving Listeria monocytogenes--role of the H-2 gene complex.
This study reports on the in vitro interactions between T cells from Listeria-immunized mice, macrophages from normal mice, and heat-killed Listeria organisms. This interaction was assayed either by determing the amount of thymocyte mitogen in culture fluids after 24 hr, or by estimating the degree of T cell proliferation after 96 hr. Each assay depended on critical concentrations of macrophages, T cells, and heat-killed Listeria, points that were evaluated in a number of experiments. Both assays required specific Listeria-immune T cells. For an effective interaction, the T cells and the macrophages had to share the I-A region of the H-2 gene complex. Macrophages bearing Ia, which represented a minor population of macrophages, were essential for the proliferative response to macrophage-associated Listeria. Also, Ia-bearing macrophages were an important component in the interactions leading to increased secretion of mitogen. The immunogenic moiety associated with Listeria was short-lived, disappearing 24 hr after uptake of Listeria by macrophages. The interactions were not blocked by anti-Listeria antibodies but were partially sensitive to trypsinization.
Animals↗
Interaction of Listeria monocytogenes and influenza in an animal model.
This study was designed to investigate the effects of viruses in the pathogenesis of Listeria monocytogenes. The organisms used in this study were: Listeria monocytogenes Type 1 isolated from a local fatal case; Mouse adapted influenza A/PR8/34 (HONI); Streptococcus pneumoniae Group B (U.M. Med. Ctr.) and poliovirus Type 2 MEF--G3M2. Balb-C mice were inoculated intraperitoneally with one LD50 of Listeria monocytogenes. Ten days later, the survivors were challenged intransally with 10 LD50 of influenza virus and observed for 14 days. Another set of Balb-C mice was inoculated intranasally with one LD50 of influenza virus and the survivors challenged 14 days later intraperitoneally with 10 LD50 of Listeria monocytogenes. Controls consisted of similar inoculation and challenge methods in mice using Streptococcus pneumoniae and polio virus with Listeria monocytogenes and influenza virus. Cross protection was observed only between Listeria monocytogenes and influenza virus. Cellular immunity may play a role in this interaction. This findings seem to agree with reports from others who showed cross protection between Listeria monocytogenes and other intracellular bacteria and parasites.
Administration, Intranasal↗
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↗
Listeria cerebritis: relapse of infection in renal transplant patients.
In 3 cases of Listeria cerebritis, two of the patients had relapse with cerebritis after antimicrobial therapy for acute Listeria septicemia or meningitis. Each had received ten to 14 days of intravenous penicillin. Relapse occurred with fever and sudden focal cerebral dysfunction. Brain scans showed focal uptake; arteriograms and computerized tomography were normal. Cerebrospinal fluids were nondiagnostic; blood cultures yielded Listeria in two patients. Penicillin treatment for six weeks produced rapid clinical responses that were complete in one and minimal residual in two. Progress brain scans were normal. A relapse rate of 35% is reported in transplant patients with Listeria meningitis and/or bacteremia who are treated for less than three weeks; to our knowledge, cerebritis in such patients has not been reported previously. High-dose penicillin or ampicillin therapy for four to six weeks is recommended for Listeria infections in this select group.
Adult↗
Immunopeptidomics Mapping of Listeria monocytogenes T Cell Epitopes in Mice.
Listeria monocytogenes is a foodborne intracellular bacterial model pathogen. Protective immunity against Listeria depends on an effective CD8+ T cell response, but very few T cell epitopes are known in mice as a common animal infection model for listeriosis. To identify epitopes, we screened for Listeria immunopeptides presented in the spleen of infected mice by mass spectrometry-based immunopeptidomics. We mapped more than 6000 mouse self-peptides presented on MHC class I molecules, including 12 high confident Listeria peptides from 12 different bacterial proteins. Bacterial immunopeptides with confirmed fragmentation spectra were further tested for their potential to activate CD8+ T cells, revealing VTYNYINI from the putative cell wall surface anchor family protein LMON_0576 as a novel bona fide peptide epitope. The epitope showed high biological potency in a prime boost model and can be used as a research tool to probe CD8+ T cell responses in the mouse models of Listeria infection. Together, our results demonstrate the power of immunopeptidomics for bacterial antigen identification.
Animals↗
Use of a macrophage cytotoxicity system to show macrophage activation by Listeria monocytogenes cell wall fraction.
Experiments were conducted to determine whether a partially purified listeria cell wall fraction could stimulate macrophages to high levels of activation. To detect activation of macrophages, a macrophage-mediated cytotoxicity system were established. The data demonstrate that listeria cell wall components are capable of activating thioglycollate-induced adherent peritoneal exudate cells to be cytotoxic for 51Cr-labelled target tumour cells, and that the listeria fraction is as effective as bacterial lipopolysaccharide in inducing cytotoxicity. The listeria fraction can also induce peritoneal exudate cells from congenitally thymusless nude mice to become cytotoxic, suggesting that mature T cells are not required. Furthermore, thioglycollate-induced adherent peritoneal exudate cells from mice hyperimmunized to live Listeria organisms are already stimulated to be cytotoxic for tumour cells, and do not need to be activated in vitro. Additional data are presented which characterize the system. These data demonstrate that a critical concentration of adherent peritoneal cells is required for in vitro activation. Moreover, only peritoneal cells induced with aged batches of thioglycollate, and not uniduced peritoneal cells or those induced with fresh thioglycollate or with protease peptone can be activated in vitro to kill tumour cells. Evidence is presented which suggests that the cytotoxic cell is a macrophage.
Animals↗
Antitumor activity of Listeria monocytogenes on a guinea pig fibrosarcoma.
Listeria monocytogenes-mediated tumor inhibition was studied in strain 13 guinea pigs by using a methylcholanthrene-induced fibrosarcoma (MCA-1). Mixtures of Listeria and tumor cells in ratios of 1:100, 1:200, or 1:400 (Listeria:MCA-1 cells) led to significant suppression of tumor growth. Intralesional injection of tumors on day 6 posttransplantation led to the regression of a highly significant number of tumors. Animals receiving injections of Listeria, either in a mixture with tumor cells or intralesionally, displayed enhanced skin test reactivity to a tumor extract. Tumor regressors were resistant for at least 2 to 3 months after the initial transplant to rechallenge with MCA-1 cells. Thus, with this particular tumor-host system, Listeria was successfully employed as an antitumor agent with no visibly detrimental side effects to the host.
Animals↗
Delayed-type hypersensitivity and acquired cellular resistance in mice immunized with killed Listeria monocytogenes and adjuvants.
Delayed-type hypersensitivity (DH) and acquired cellular resistance (ARC) to Listeria monocytogenes in mice was studied following immunization with killed bacteria in combination with Freund's complete adjuvant or the adjuvant dimethyldioctadecylammonium bromide (DDA). Intracutaneous or intraperitoneal injections of killed listeria mixed with Freund's complete adjuvant did neither result in DH nor in ACR. Intracutaneous injections of killed listeria and DDA resulted in an antigen-dose dependent DH but not in ACR. Intraperitoneal injections of listeria and DDA, however, induced ACR but no DH. Optimal conditions for the induction of ACR were simultaneous intraperitoneal injection of 15 mg DDA/kg body weight and 10(7) or 10(8) listeria. The optimal interval between immunization and challenge was 7 days. No protection was found against challenge with a lethal dose of Salmonella enteritidis, suggesting that the protection is specific. Intraperitoneal injection of mice with DDA resulted in inhibition of phagosome-lysosome fusion in macrophages harvested 24 h later. Interference with macrophage activity is discussed as one of the possible mechanisms for the adjuvant effect of DDA.
Adjuvants, Immunologic↗
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↗
[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↗
[Resistance to infection with Listeria monocytogenes in normal and thymusless mice treated with ampicillin (author's transl)].
NMRI mice were infected intravenously with a sublethal dose of Listeria monocytogenes and divided into four groups. One group served as the control and the other three were treated with ampicillin beginning 4, 8 or 24 hours after infection. The animals were injected in the morning and in the evening each time with 4 mg ampicillin subcutaneously until a total dose of 48 mg was reached. As demonstrated by counting of the bacteria in the spleen, Listeria could multiply in the ampicillin treated mice in comparison to the control group at best delayed but the infection continued to persist for some days at a level of 10(3)-10(4) Listeriae per spleen independent from the starting point of the treatment. Eight days after the first infection all animals received a challenge dose of 10(4) Listeriae. Compared with the control animals the ampicillin treated mice had a clearly reduced immunity, even in the group in which ampicillin application had been started 24 hours after the primary infection. If the challenge infection was given at first after an intervall of six weeks between primary and secondary infection, only a reduced immunity was found. Furthermore, whereas spleen cells of mice 7 days after infection were able to transfer immunity to untreated recipients, spleen cells of ampicillin treated mice were unable to do so. Finally, an attempt was made to cure chronic listeric infection in thymusless nude mice by the application of high doses of ampicillin. The observation of a continuous infection in these animals showed that the T-cells played a primary importance in the elimination of the bacteria.
Ampicillin↗
Resistance to Listeria monocytogenes in mice: genetic control by genes that are not linked to the H-2 complex.
After mice of several inbred strains were injected with Listeria monoyctogenes, two parameters of resistance, the 50% lethal dose and the suppression of bacterial proliferation in spleen, were determined. The strains of mice tested could be segregated into two groups: the resistant C57BL/10Sn mice and the sensitive A/J and DBA/2J mice. Congenic resistant strains of mice were used because they would express the H-2 haplotype of the sensitive strains (H-2a or H-2d) on the background of a resistant strain, C57BL/10Sn. Both the B10.A/SgSn (H-2a) and the B10.D2/Sn (H-2d) mice were as resistant as mice from their background strain and were significantly more resistant than the strains that donated their H-2 locus (A/J or DBA/2J). Therefore, the resistance of mice to Listeria, although genetically controlled, is not controlled by gene (s) linked to the H-2 haplotype. On the other hand, the level of specific immunity to listeria antigens (as indicated by the footpad reaction) was higher in the C57BL/10Sn (H-2b) mice than in either the A/J and B10.A/SgSn (H-2a) mice or the DBA/2J and B10.D2/Sn (H-2d) mice. This observation suggests an H-2 linkage of specific immunity to Listeria.
Animals↗
Listeria monocytogenes: brain abscess or meningoencephalitis?
A brain abscess caused by Listeria monocytogenes developed in an immunosuppressed renal transplant patient. Meningitis and meningoencephalitis from this organism were encountered in three other renal transplant recipients at this medical center during the past 4 years. Focal neurologic deficits occurred in patients with either Listeria abscess or meningoencephalitis. Computerized tomography was a rapid aid to the diagnosis of abscess. Immunosuppression has increased the incidence of central nervous system Listeria infections, but ampicillin still provides effective treatment, even when immunosuppressive therapy is continued. Limited experience with Listeria brain abscess suggests that surgical intervention improves the prognosis.
Adult↗
Listeria encephalitis in five renal transplant recipients.
Listeria encephalitis has occurred recently in 5 renal transplant recipients at the Transplantation Unit in Stockholm. Symptoms from the central nervous system, such as coma, hemiparesis and cranial nerve paresis, dominated the clinical picture. Listeria monocytogenes was isolated from the blood of all the patients, from the cerebrospinal fluid in two, from the urine in one and post mortem from the brain in one patient. Pleocytosis never exceeded 200 leucocytes/mm3 and the glucose ratio was normal or near normal. Complement fixation test for Listeria was negative in all 5 patients. Four patients expired in spite of treatment with large doses of penicillin and other antibiotics to which the isolated strains were sensitive in vitro. At autopsy, inflammation and necrosis were observed in the brain, especially the brain stem, and there was mild lymphocytic infiltration of the meninges. The surviving patient was treated with a combination of chloramphenicol and ampicillin.
Adult↗