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PubMed2003

Listeria monocytogenes infection as a complication of treatment with tumor necrosis factor alpha-neutralizing agents.

OBJECTIVE: Tumor necrosis factor alpha (TNFalpha) has been implicated in the pathogenesis of certain inflammatory diseases. Two TNFalpha-neutralizing agents are licensed in the US. Infliximab is licensed for the treatment of Crohn's disease (CD) and, when used with methotrexate, for the treatment of rheumatoid arthritis (RA). Etanercept is licensed for the treatment of RA, including juvenile RA, and, more recently, was licensed for the treatment of psoriatic arthritis. Because of the potential for decreased host resistance to infectious agents due to treatment with anti-TNFalpha agents, we sought to evaluate postlicensure cases of opportunistic infection, including Listeria monocytogenes, in patients treated with these products. METHODS: The FDA Adverse Event Reporting System, a passive monitoring system, was reviewed to identify all reports of adverse events (through December 2001) associated with L monocytogenes infection in patients treated with infliximab or etanercept. RESULTS: Fifteen cases of L monocytogenes infection associated with infliximab or etanercept treatment were identified. In 14 of these cases, patients had received infliximab. The median age of all patients was 69.5 years (range 17-80 years); 53% were female. Six deaths were reported. Among patients for whom an indication for use was reported, there were 9 patients (64%) with RA and 5 patients (36%) with CD (information was not reported for 1 patient). All patients for whom information was reported were receiving concurrent immunosuppressant drugs. CONCLUSION: Postlicensure surveillance suggests that L monocytogenes infection may be a serious complication of treatment with TNFalpha-neutralizing agents, particularly infliximab.

Adolescent↗
PubMed1989

Recombinant murine gamma interferon induces enhanced resistance to Listeria monocytogenes infection in neonatal mice.

Neonatal mice within 24 h of birth were highly susceptible to intraperitoneal infection with Listeria monocytogenes. The 50% lethal dose of bacterial cells was 6.3 X 10(1) CFU for neonates and 3.2 X 10(6) CFU for adult mice. A single injection of recombinant murine gamma interferon (rMuIFN-gamma) protected neonatal mice from simultaneous challenge with a lethal dose of L. monocytogenes cells. The rMuIFN-gamma effect was dose dependent: protection was consistently observed in mice treated with rMuIFN-gamma at doses of more than 4 X 10(2) U (0.1 microgram of protein) per mouse. Bacterial growth in the spleens and livers of rMuIFN-gamma-treated neonates was significantly suppressed in comparison with that in the nontreated controls. The infected neonatal mice showed acquired antilisterial resistance against secondary intravenous infection after 4 weeks of age, and this resistance was significantly augmented in mice that had been treated with rMuIFN-gamma.

Adjuvants, Immunologic↗
PubMed1986

Monocyte migration explains the changes in macrophage arachidonate metabolism during the immune response.

The profile of arachidonic acid metabolites in resident peritoneal macrophages is distinctly different from the profile of macrophages isolated after an acute bacterial infection. The latter produce decreased prostaglandins E2 and I2 and leukotriene C4 while conserving the synthesis of thromboxane A2. We show here that the initial changes in peritoneal macrophage arachidonate metabolism during the immune response appear to be the result of the large influx of blood monocytes, which have a characteristic metabolism distinct from resident macrophages. We demonstrate that the initial decrease in peritoneal macrophage arachidonate metabolism and the increase in macrophage numbers occur simultaneously after infection with Listeria monocytogenes. Also the macrophage arachidonate metabolism seen at the height of the peritoneal cellular influx is the same as that of purified blood monocytes. Both Listeria peritoneal macrophages and blood monocytes produce equal or greater quantities of thromboxane A2 relative to prostaglandins I2 and E2 or leukotriene C4 whereas resident cells produce 1/10 to 1/25 as much thromboxane A2 compared to the other products. Furthermore, the changes in peritoneal macrophage arachidonate metabolism in response to Listeria infection do not occur if the influx of blood monocytes is stopped by irradiating the mice prior to infection implying that the cellular influx is necessary to see the changes in arachidonate metabolism. Finally, activation of peritoneal macrophages, measured as an increase in Ia expression, occurs 36 hr after the influx of monocytes from the blood and the resultant shift in arachidonate metabolism during Listeria infection.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Listeria Monocytogenes infections.

This article reviews current information regarding human infection with Listeria monocytogenes. Significant advances have occurred in regard to our knowledge of the epidemiology, pathogenesis, immunology, and treatment of this disease which was formerly believed to be of importance mainly to veterinarians. It remains a cause of high mortality in the many different groups of compromised hosts it infects unless diagnosis and treatment are rapidly established.

Adult↗
PubMed1999

Endogenous cytokines during a lethal infection with Listeria monocytogenes in mice.

It has been demonstrated that endogenous cytokines including gamma interferon (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) play protective roles but that IL-4 and IL-10 play detrimental roles in nonlethal Listeria monocytogenes infection in mice. In this paper, we studied the roles of endogenous cytokines in a lethal infection with L. monocytogenes in mice. TNF-alpha and IL-6 titres in the bloodstreams, spleens and livers paralleled bacterial numbers in the organs, and both these cytokines and the bacterial numbers peaked just before the mice died. The high titres of TNF-alpha notably detected in the circulation in lethal infection were different from those in nonlethal infection. The maximum production of IFN-gamma was observed before the peaks of TNF-alpha and IL-6, and IFN-gamma almost disappeared from the bloodstreams and organs just before the mice died. No notable difference of IFN-gamma titres between lethal infection and nonlethal infection in the specimens obtained from mice was observed. IL-10 was also detected in the bloodstreams earlier than the peaks of TNF-alpha and IL-6 during lethal infection, while IL-4 was never detected in the sera. The administration of monoclonal antibodies (mAbs) against TNF-alpha, IFN-gamma, IL-6, IL-4 or IL-10 failed to rescue mice from lethal L. monocytogenes infection, whereas anti-TNF-alpha mAb and anti-IFN-gamma mAb prevented mice from lethality by high-dose endotoxin shock. These results suggest that lethality in L. monocytogenes infection might not be determined solely by these cytokines.

Animals↗
PubMed1996

Endogenous interleukin-4, but not interleukin-10, is involved in suppression of host resistance against Listeria monocytogenes infection in interferon-depleted mice.

The production and roles of endogenous interleukin-4 (IL-4) and IL-10 in a sublethal infection with Listeria monocytogenes were studies in normal mice and anti-gamma interferon (IFN-gamma) monoclonal antibody (MAb)-pretreated mice. In normal mice, the expression of mRNAs for IL-4 and IL-10, which was amplified by reverse transcription-PCR, was induced in the spleens and livers either early or late in infection, although the serum IL-4 and IL-10 were not detectable by enzyme-linked immunosorbent assays. In vivo administration of anti-IL-4 MAb showed no effect on antilisterial resistance, whereas anti-IL-10 MAb partially diminished the defense. In anti-IFN-gamma MAb-pretreated mice, a delay in the bacterial elimination from the spleens and livers was observed and high titers of serum IL-4 and IL-10 were induced late in infection. Production of endogenous IL-4 and IL-10 was suppressed in both CD4+ cell-and CD8+ cell depleted mice. The suppression of antilisterial resistance in anti-IFN-gamma MAb-pretreated mice was canceled when anti-IL-4 MAb was injected late in infection, whereas anti-IL-10 MAb showed no effect. These results suggest that the host immune responses were polarized into the T-helper 2 phenotype in anti-IFN-gamma MAb-pretreated mice and that inhibition of host resistance against L. monocytogenes by depletion of IFN-gamma might be attributable to IL-4 produced by T cells polarized into the T-helper 2 phenotype as well as the inhibition of the IFN-gamma effects.

Animals↗
PubMed2002

Extensive and preferential Fas/Fas ligand-dependent death of gammadelta T cells following infection with Listeria monocytogenes.

In the spleens of mice infected intraperitoneally with the bacterium Listeria monocytogenes, both alphabeta and gammadelta T cells became rapidly activated, followed by a massive apoptotic death response predominantly within the gammadelta population. The death response involved two major splenic gammadelta T-cell subsets and was Fas/Fas ligand (Fas-L)-dependent. Among T cells isolated from the Listeria-infected spleen, Fas-L was almost exclusively expressed in gammadelta T cells. gammadelta T cells coexpressed Fas and Fas-L, suggesting activation-induced suicide as a mechanism of their death. In vivo treatment with an antibody specific for CD3epsilon induced activation, preferential Fas-L expression and apoptosis of gammadelta T cells, resembling the response pattern in listeriosis, whereas antibodies specific for T-cell receptor-beta (TCR-beta) or TCR-delta did not, suggesting that the complete response seen in listeriosis requires both gammadelta TCR engagement and additional stimuli. L. monocytogenes causes early nonspecific, Fas-independent lymphocyte death in heavily infected tissues. In contrast, the death response described here is selective, Fas-dependent and triggered at low local levels of bacteria, suggesting that it is controlled by interactions with other infection-activated host cells, and perhaps part of a regulatory circuit specifically curtailing gammadelta T cells.

Animals↗
PubMed1997

In vivo and in vitro activation and expansion of gammadelta T cells during Listeria monocytogenes infection in humans.

Serial flow cytometry analyses of peripheral blood mononuclear cells obtained from 8 patients infected with Listeria monocytogenes showed a higher percentage (P < 0.01) of gammadelta T cells (median, 11.7; range, 3.7 to 35.3) than did 16 age-matched uninfected controls (1.7, 0.4 to 13). Most in vivo-expanded gammadelta T cells expressed the Vgamma9 and Vdelta2 gene products and displayed a memory phenotype (CD45RO[high]), and patients' gammadelta T cells expressed significantly more (P < 0.01) activation marker HLA-DR than did controls (19.8% [median] and 0.9 to 87.6% [range] versus 2.3% and 0 to 4.7%, respectively). When peripheral blood mononuclear cells from normal donors were cultured in vitro with heat-killed Listeria cells, analysis of CD25 and HLA-DR expression on gammadelta and alphabeta T cells indicated that a high percentage of gammadelta T cells was activated early compared to alphabeta T cells. In addition, depletion of gammadelta T cells before culture abrogated the early lymphocyte proliferative response induced by the pathogen. Taken together, these results argue for the involvement of gammadelta T cells during L. monocytogenes infection in humans.

Adult↗
PubMed2001

Organ-specific regulation of the CD8 T cell response to Listeria monocytogenes infection.

The intestinal mucosal CD8 T cell response to infection with Listeria monocytogenes was measured using MHC class I tetramers and was compared with the response in peripheral blood, secondary lymphoid tissue, and liver. To assess the vaccination potential of Listeria and to analyze responses in C57BL/6 mouse strains, a recombinant Listeria expressing OVA (rLM-ova) was generated. The response peaked at 9 days postinfection with a much larger fraction of the intestinal mucosa and liver CD8 T cell pool OVA specific, as compared with the spleen. However, these differences were not linked to bacterial titers in each site. The higher responses in lamina propria and liver resulted in a larger CD8 memory population in these tissues. Furthermore, the level of memory induced was dependent on infectious dose and inversely correlated with the magnitude of the recall response after oral challenge. Recall responses in the tissues were most robust in the lamina propria and liver, and reactivated Ag-specific T cells produced IFN-gamma. Infection of CD40- or MHC class II-deficient mice induced poor CD8 T cell responses in the intestinal mucosa, but only partially reduced responses in the spleen and liver. Overall, the results point to novel pathways of tissue-specific regulation of primary and memory antimicrobial CD8 T cell responses.

Administration, Oral↗
PubMed1998

Disruption of the cellular inflammatory response to Listeria monocytogenes infection in mice with disruptions in targeted genes.

The results of this study to dissect the nature of the acquired immune response to infection with Listeria monocytogenes in mice with targetted gene disruptions show that successful resolution of disease requires the essential presence of alphabeta T cells and the capacity to elaborate gamma interferon. In the absence of either of these entities, mice experience increasingly severe hepatitis and tissue necrosis and die within a few days. The data from this study support the hypothesis that the protective process is the efficient replacement of neutrophils in lesions by longer-lived mononuclear phagocytes; alphabeta-T-cell-knockout mice died from progressive infection before neutrophil replacement could occur, whereas in gammadelta-T-cell-knockout mice this replacement process in the liver has previously been shown to be much slower. In the present study we attribute this delay to reduced production of the macrophage-attracting chemokine MCP-1 in the gammadelta-T-cell-knockout animals. These data further support the hypothesis that gammadelta T cells are important in controlling the inflammatory process rather than being essential to the expression of protection.

Animals↗
PubMed1992

Listeria monocytogenes infection in prosthetic joints.

Listeria monocytogenes is increasingly recognised as a cause of prosthetic joint infection. These infections tend to be more insidious and indolent in contrast to similar infections with Staphylococcus aureus. They can occur in patients who are immunocompromised due to malignancy or other illness or in nonimmunocompromised elderly patients. Listeria infections should not be treated with cephalosporins and prolonged antimicrobial treatment is generally advised for prosthetic joint infections. We noted a high affinity of L. monocytogenes for foreign bodies. Three of twenty-seven cases 11%) of listeriosis under the period of investigation were associated with foreign bodies (hip prosthesis, knee prosthesis and arterial graft).

Aged↗
PubMed1993

Free versus liposome-encapsulated muramyl tripeptide phosphatidylethanolamide (MTPPE) and interferon-y (IFN-y) in experimental infection with Listeria monocytogenes.

The effect of free and liposome-encapsulated muramyl tripeptide phosphatidylethanolamide (MTPPE) and interferon-y (IFN-y) on the resistance against Listeria monocytogenes infection in mice was investigated. It was shown that administration of MTPPE or IFN-y at 24 h before bacterial inoculation led to increased resistance against L. monocytogenes infection in terms of a decrease in bacterial numbers in liver and spleen. Encapsulation of MTPPE and IFN-y in liposomes increased their efficacy 33- or 66-fold, respectively. In addition, liposomal encapsulation led to a more rapid decrease in bacterial numbers. The immunomodulator to lipid ratio appeared to be very important in the antibacterial effect of LE-MTPPE and LE-IFN-y. When nontherapeutic doses of liposome-encapsulated MTPPE or IFN-y were administered in a larger amount of lipid (so at higher lipid: immunomodulator ratio), these doses became effective. Exposure of macrophages in monolayer infected with L. monocytogenes in vitro to MTPPE had no effect, whereas exposure to IFN-y only led to growth inhibition of the intracellular bacteria. However, incubation of macrophages with a combination of MTPPE and IFN-y resulted in killing of the intracellular bacteria. Exposure of macrophages in vivo to both immunomodulators in combination can be effected by using liposomes as carriers. It was observed that administration of MTPPE and IFN-y co-encapsulated in liposomes resulted in a synergistic enhanced antibacterial resistance against L. monocytogenes. Both reactive oxygen and nitrogen intermediates seemed to play a role in the killing of L. monocytogenes by macrophages activated with a combination of MTPPE and IFN-y.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1998

Restraint stress-induced immunosuppression by inhibiting leukocyte migration and Th1 cytokine expression during the intraperitoneal infection of Listeria monocytogenes.

In this study, a murine model of Listeria monocytogenes infection was used to investigate effects of restraint stress (RST) on host defense. We observed that the L. monocytogenes infection as well as RST induced an elevation of endogenous corticosterone (CORT) levels and RST synergistically enhanced endogenous CORT levels during the listerial infection. RST suppressed the migration of leukocytes including macrophages, neutrophils, NK cells and lymphocytes into the peritoneal cavities after the intraperitoneal inoculation of L. monocytogenes. RST also suppressed the increase of the surface MHC class II antigen expression in both peritoneal macrophages and B cells during the listerial infection. Interestingly, gene expression of iNOS, MCP-1 (JE) and Th1-type cytokines including IFN-gamma and IL-12 was down-regulated but Th2-type cytokine (IL-4 and IL-6) gene expression in the PEC was rather up-regulated on day 7 after infection, indicating that Th2-type immune response is more resistant to the elevated endogenous CORT levels than Th1-type response. Treatment of mice with RU486, a glucocorticoid receptor antagonist, restored the immune responses suppressed by RST to their normal levels in the infected mice, suggesting that the RST-induced elevation of endogenous corticosterone levels is mainly responsible for the induction of the immunosuppressive events during L. monocytogenes infection.

Animals↗
PubMed1997

Effect of experimental infection with Listeria monocytogenes on the development of pregnancy and on concentrations of progesterone, oestrone sulphate and 15-ketodihydro-PGF2 alpha in the goat.

The effect of Listeria monocytogenes infection on hormone levels in pregnant goats was studied. Four goats (Group I) received an intravenous inoculation of a bacterial culture (Type 1) on Days 69-77 and another four goats (Group II) received a similar inoculation on Days 105-106 of gestation. Five non-inoculated goats were used as controls. Plasma was analysed for progesterone, oestrone sulphate and 15-ketodihydro-PGF2 alpha. The status of the foetus was followed using real-time ultrasonography. Three of the four goats in Group I aborted 8-10 days after inoculation. The fourth goat gave birth to a normal live kid at term. The three goats which aborted showed clinical signs of disease in connection with abortion. In Group II, all goats aborted after 9-11 days. All the goats showed clinical symptoms of disease from a few days after inoculation and the symptoms continued until abortion. The clinical symptoms of disease were more pronounced in Group II than in Group I. L. monocytogenes was isolated from all aborted foetuses. None of the control goats aborted. Ultrasound examination revealed foetal death either immediately before or up to 2 days before abortion. Mummification had begun in the foetus that had been dead for 2 days before expulsion. In comparison with pre-inoculation plasma levels in Group I, a significant decrease (P < 0.05) in progesterone levels and an increase in 15-ketodihydro-PGF2 alpha levels were observed from Days 4 and 6 after inoculation, respectively. In Group II, a significant decrease (P < 0.05) in progesterone levels and an increase in 15-ketodihydro-PGF2 alpha levels in plasma were observed from Days 8 and 6, respectively. The oestrone sulphate levels decreased slightly in the inoculated goats a few days before abortion. The pattern of changes in levels around abortion was similar to the pattern present in the control animals around parturition. However, oestrone sulphate levels did not increase in the inoculated groups before abortion in contrast to goats which delivered healthy kids. The changes in levels of 15-ketodihydro-PGF2 alpha in goats that aborted indicated that the endocrine foetal-placental function was disturbed, which was most likely due to the establishment and development of L. monocytogenes in the placenta and foetus.

Animals↗
PubMed1992

The protective activity of immunostimulants against Listeria monocytogenes infection in mice.

The function of peritoneal macrophages induced by intraperitoneal (i.p.) injection of attenuated Streptococcus pyogenes (OK-432), Bacillus Calmette Guérin (BCG), protein-bound polysaccharide preparation isolated from Coriolus vesicolor (PSK) or Lactobacillus casei was examined. The PMA-triggered respiratory burst (production of O2- and H2O2) of macrophages induced by OK-432, BCG or Lac. casei was greater than that of resident or thioglycollate-stimulated macrophages and was similar to that of BCG-activated macrophages. PSK failed to enhance the production of O2- or H2O2 by macrophages. Alkaline phosphodiesterase (APD) activity was reduced in macrophages induced by OK-432, BCG or Lac. casei injection and in BCG-activated macrophages. The APD activity of macrophages obtained 7 and 13 days after i.p. injection of PSK was elevated, as with thioglycollate-stimulated macrophages. Listericidal activity in vitro was enhanced in macrophages obtained in 13 and 7 days, but suppressed in macrophages obtained 2 days after OK-432, BCG or Lac. casei injection. Lac. casei administered either 2 or 13 days before infection with Listeria monocytogenes was protective but OK-432, BCG (0.1 mg) and PSK were not, even though they were able to stimulate macrophage function.

Adjuvants, Immunologic↗
PubMed1996

The protective role of endogenous cytokines in host resistance against an intragastric infection with Listeria monocytogenes in mice.

It has been demonstrated that endogenous cytokines including gamma-interferon (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6) play a protective role but that IL-4 plays a detrimental role in systemic Listeria monocytogenes infection in mice. The diverse roles of IL-10 have been reported in antilisterial resistance. In this paper, we studied the role of endogenous cytokines in host resistance against an intragastric infection with L. monocytogenes in mice. The expression of cytokine mRNAs including IFN-gamma, TNF-alpha, IL-4, IL-6, or IL-10, which were amplified by reverse transcription-PCR, was observed in intestinal intraepithelial lymphocytes irrespective of L. monocytogenes infection. Increased numbers of L. monocytogenes were detected in the ileal contents of infected mice which received monoclonal antibodies (mAbs) against IFN-gamma, TNF-alpha, IL-4, IL-6, or IL-10. By contrast, mAbs against IL-4 or IL-6 showed little effect on the growth of L. monocytogenes in the mesenteric lymph nodes (MLNs), spleen, and liver, but anti-IFN-gamma mAb and anti-TNF-alpha mAb suppressed the defense in these organs. Anti-IL-10 mAb enhanced bacterial elimination from the MLNs but not from the spleen or liver. These results suggest that the role of endogenous cytokines may differ between systemic and intestinal defenses.

Animals↗
PubMed1987

Gamma interferon-mediated increase in the number of Ia-bearing macrophages during infection with Listeria monocytogenes.

The role of gamma interferon (IFN-gamma) in an increase in Ia-bearing macrophages during Listeria monocytogenes infection was studied. The peritoneal macrophages from L. monocytogenes-infected mice contained a high proportion of Ia. Intraperitoneal injection of the supernatant from a culture of spleen cells from L. monocytogenes-infected mice induced Ia-rich exudates in normal mice. The Ia-inducing activity in the culture supernatant was abrogated by the pretreatment of spleen cells with anti-Thy-1.2 antibody plus complement. Immunoadsorption of the culture supernatant with anti-recombinant IFN-gamma antibody and protein A-Sepharose CL-4B completely abrogated its Ia-inducing activity. These results suggested that an increase in Ia-bearing macrophages during L. monocytogenes infection was attributable to T-cell-derived IFN-gamma.

Animals↗
PubMed1989

Protection of mice against Listeria monocytogenes infection by recombinant human tumor necrosis factor alpha.

Recombinant human tumor necrosis factor alpha (rHuTNF-alpha) administered intravenously to mice resulted in enhanced resistance to a lethal challenge infection of Listeria monocytogenes given 24 h later. The observed protection was lost following treatment of the rHuTNF-alpha preparations with rabbit polyclonal antibody rHuTNF-alpha but not with normal rabbit immunoglobulin G.

Animals↗