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Results for “LISTERIA INFECTIONS”

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At least 19 recordsLinked to original sources
PubMed2005

A defective Th1 response of the spleen in the initial phase may explain why splenectomy helps prevent a Listeria infection.

Listeria monocytogenes (Listeria) are known to grow and proliferate in the liver while a splenectomy induces host resistance against a Listeria infection despite the fact that a splenectomy inhibits the Th1 response. Therefore, the mechanism by which a splenectomy helps to prevent the growth of Listeria still remains to be elucidated. After an i.v. challenge of Listeria (1 x 10(6) CFU) in C57BL/6 mice, Listeria rapidly increased in the spleen but not in the liver until 48 h. However, after this initial phase, Listeria remarkably grew in the liver. In contrast, when the mice received a splenectomy beforehand, no remarkable growth of Listeria in the liver was observed after Listeria challenge despite the fact that serum IFN-gamma and IL-12 levels at 24 h after Listeria challenge were significantly lower than those in the sham mice. However, the liver leucocytes from mice by 6 h after infection produced a substantial amount of IFN-gamma while spleen MNC did not, whereas spleen leucocytes at 24 h after Listeria challenge did. Consistently, the IFN-gamma and IL-12 levels in the tissue homogenates of the spleen were significantly lower than in those of the liver until 6 h after infection. This defective spleen Th1 response in the early phase of Listeria infection was corrected by an IL-18 i.p. injection just after the Listeria challenge. Our findings suggest that Listeria exploit the defective Th1 environment of the spleen in the initial phase and afterwards overcome the host defense mechanism of the liver.

Animals↗
PubMed1999

The mucosal phase of Listeria infection.

Listeria monocytogenes is an enteroinvasive bacterial pathogen of man and animals. Listeriae have been shown capable of infecting the host by translocating from the intestinal lumen through Peyer's Patches (PP), however, results of experiments now indicate that these facultative intracellular parasites may also translocate through PP-independent routes. With regards to this, on occasion we observed that listeriae were absent from the PP of mice inoculated intragastrically with L. monocytogenes, but were present in the mesenteric lymph nodes of these same mice. These observations suggested that PP were not necessary for listerial translocation from the intestinal lumen. Two experimental approaches were used to determine whether luminal listeriae could indeed infect the host through PP-independent routes. First, since it is known that: 1) following the intragastric inoculation of L. monocytogenes, listeriae rapidly transit the length of the gastrointestinal tract and reside in the colonic lumen for up to a week, 2) the colon lacks PP, and 3) the descending colon and rectum are drained exclusively by the caudal lymph node (CLN), it was determined whether colonic listeriae could access the CLN. Inoculation of listeriae into the rectum of mice resulted in the infection of the CLN which indicated that PP were not required for listerial translocation. Second, since germfree SCID mice lack PP, it was determined whether listeriae could translocate from the intestinal lumen and infect these immunoincompetent mice. Shortly after the intragastric inoculation of L. monocytogenes into germfree SCID mice, listeriae were found in the mesenteries, livers and spleens. These results also indicate that PP are not required for listerial translocation from the intestinal lumen. One possible route of translocation from the intestinal lumen might occur by listeriae entering enterocytes. Results were obtained showing that listeriae were capable of entering cultured mouse small intestine enterocytes. Internalized listeriae were observed to multiply and spread intracellularly between enterocytes.

Animals↗
PubMed1995

[A new case of arterial Listeria infection].

Listeria monocytogenes arterial infections are uncommon and usually occur on aneurysms of previously operated arteries, classically in very young and very old or immunodepressed subjects. Peroperative samples for bacteriology should always be taken as antibiotics generally used in vascular surgery are ineffective against listeria. We report a case of a patient who underwent emergency surgery. Bacteriologic analysis of the thrombus revealed listeria inoculation which was eradicated by adapted antibiotic treatment.

Aged↗
PubMed2001

Two novel genes FIND and LIND differentially expressed in deactivated and Listeria-infected human macrophages.

Deactivation of macrophage functions plays an important role in human infectious and inflammatory diseases. In this study, differential-display RT-PCR was used to analyze the gene expression of human mononuclear phagocytes deactivated with interleukin (IL)-4, IL-10, and dexamethasone (DEX), in the absence and presence of infection with Listeria monocytogenes (Listeria). Two novel differentially expressed mRNA species were discovered: FIND (IL-Four INDuced) was upregulated with IL-4 but down-regulated with DEX, and is predicted to code for an M(r) 53,000 transmembrane protein. LIND (Listeria INDuced) was induced by Listeria infection, and is predicted to code for an M(r) 39,000 nuclear or cytoplasmic protein containing three coiled-coil domains. In addition, we report several novel effects of deactivators and infection on the expression of known genes: (1) IL-4 caused pronounced upregulation of ABCG2, coding for an ATP-binding cassette transporter highly expressed in the placenta, which mediates multidrug resistance of cancer cells, but is otherwise of unknown function; (2) both DEX and IL-4 downregulated osteopontin, an important factor of host resistance against intracellular infections; (3) inhibition of the CC-chemokine I-309 mRNA expression by all three deactivators in the presence of Listeria infection, and (4) upregulation by Listeria infection of the interferon-stimulated gene ISG20 of unknown function, whose product localizes with nuclear dots/PML bodies.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Type I interferon sensitizes lymphocytes to apoptosis and reduces resistance to Listeria infection.

Infection with Listeria monocytogenes causes lymphocyte apoptosis that is mediated by the actions of the pore-forming virulence factor listeriolysin O (LLO). Previous work showed that activated lymphocytes were highly sensitive to LLO-induced apoptosis, whereas resting lymphocytes were less susceptible. We now show that mice deficient in the type I interferon (IFN) receptor were more resistant to Listeria infection and had less apoptotic lesions than wild-type counterparts. Furthermore, treatment of resting splenic lymphocytes with recombinant IFN-alphaA enhanced their susceptibility to LLO-induced apoptosis. Together, these data suggest that type I IFN signaling is detrimental to handling of a bacterial pathogen and may enhance the susceptibility of lymphocytes undergoing apoptosis in response to bacterial pore-forming toxins.

Animals↗
PubMed1998

Listeria infection after liver transplantation: report of a case and review of the literature.

Listeria monocytogenes is a well-recognized cause of bacteremia and meningitis in immunocompromised individuals, including recipients of solid organ transplants, but has only rarely been reported following orthotopic liver transplantation (OLT). Most previously reported cases of listeriosis occurred months to years following liver transplantation; we describe a case of listeriosis that occurred within 1 wk of liver transplantation, shortly after discontinuation of trimethoprim-sulfamethoxazole prophylaxis, and review the English literature on Listeria infection after OLT. The patient developed abdominal pain and fever that suggested a bile leak, but was definitively diagnosed with Listeria infection by blood culture. The infection was successfully treated with 3 wk of intravenous ampicillin. We conclude that serious systemic infection with Listeria monocytogenes is uncommon following OLT, may occur early in the postoperative period, and responds well to treatment with high dose ampicillin.

Adult↗
PubMed2000

Immunity to Listeria infection.

Infection with Listeria monocytogenes is a well studied model for understanding host resistance to intracellular bacteria. Recent advances in the study of Listeria have carefully quantitated the response of CD8(+) T cells to infection and analyzed the effector functions of these cells in vivo. A surprising role for antibody in mediating resistance to Listeria has also recently emerged, providing new insight into the mechanisms of host defense.

Animals↗
PubMed1995

Interaction of interleukin-6, tumour necrosis factor and interleukin-1 during Listeria infection.

Injected recombinant interleukin-6 (IL-6), tumour necrosis factor (TNF) and IL-1 all protect mice against experimental infection with Listeria monocytogenes. We have therefore investigated the interaction of these cytokines during infection. Treatment with recombinant (r)IL-6 enhanced TNF production by spleen cells during the first 2 days of infection. Anti-TNF antibody could totally abolish the protective effect of rIL-6, while the optimal protective function of TNF could not be achieved when IL-6 was neutralized by anti-IL-6 antibody. IL-1 induced a high level of IL-6 in the serum a short time after its administration, and neutralization of IL-6 totally abolished the protective function of rIL-1. The results thus provide further evidence for the complexity of cytokine interaction.

Animals↗
PubMed1975

Specific immunity and nonspecific resistance to infection: listeria, protozoa, and viruses in mice and hamsters,.

Specific immunity developed by mice against protozoan (Toxoplasma gondii and Besnoitia jellisoni) and bacterial (Listeria monocytogenes) infections was compared with nonspecific protection conferred by prior infections. The results indicated that homologous immunity protected mice from more than 10-5 LD50 of T. gondii or B. jellisoni, but from only 10-2 LD50 of L. monocytogenes. Heterospecific protection among these organisms was for 10-0.4 minus 10-1.2 LD50. In studies in hamsters specific immunity to protozoan (T. gondii and B. jellisoni) and viral (equine Herpesvirus type 1 and Oriboca virus) infections was compared with nonspecific protection conferred by prior infections with several heterospecific agents: T. gondii; B. jellison; equine Herpesvirus type 1; Oriboca, Ossa, vesicular stomatitis, yellow fever, and Newcastle disease viruses; L. monocytogenes; and the bacillus Calmette-Guerin strain of Mycobacterium tuberculosis. The results indicated that homologous immunity in hamsters was effective against 10-6 minus 10-7 LD50 of T. gondii, B. jellisoni, equine Herpesvirus type 1, or Oriboca virus. Prior infection with Newcastle disease virus protected (probably by interferon induction) against 10-3 LD50 of equine Herpesvirus type 1. Heterospecific protection among other agents was for less than 10 LD50. This insignificant heterospecific protection in infections in which cellular immunity plays a role suggests that both the induction phase and the expression phase are specific.

Animals↗
PubMed2005

CpG oligodeoxynucleotides enhance neonatal resistance to Listeria infection.

Infection by Listeria monocytogenes causes serious morbidity and mortality during the neonatal period. Previous studies established that immunostimulatory CpG oligodeoxynucleotides (ODN) can increased the resistance of adult mice to many infectious pathogens, including Listeria. This work examines the capacity of CpG ODN to stimulate a protective immune response in newborns. Results indicate that dendritic cells, macrophages, and B cells from 3-day-old mice respond to CpG stimulation by secreting IFN-gamma, IL-12, and/or TNF-alpha. Spleen cells from CpG-treated neonates produce large amounts of cytokine and NO when exposed to bacteria in vitro. Newborns treated with CpG ODN are protected from lethal Listeria challenge and generate Ag-specific CD4 and CD8 T cells that afford long-term protection against subsequent infection. These results demonstrate that cellular elements of the neonatal immune system respond to stimulation by CpG ODN, thereby reducing host susceptibility to infectious pathogens.

Adjuvants, Immunologic↗