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Listeria Monocytogenes Infection (listeria + monocytogene_infection)
Selected Abstracts,-GalCer ameliorates listeriosis by accelerating infiltration of Gr-1+ cells into the liverEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2010Masashi Emoto Abstract ,-Galactosylceramide (,-GalCer) activates invariant (i)NKT cells, which in turn stimulate immunocompetent cells. Although activation of iNKT cells appears critical for regulation of immune responses, it remains elusive whether protection against intracellular bacteria can be induced by ,-GalCer. Here, we show that ,-GalCer treatment ameliorates murine listeriosis, and inhibits inflammation following Listeria monocytogenes infection. Liver infiltration of Gr-1+ cells and ,/, T cells was accelerated by ,-GalCer treatment. Gr-1+ cell and ,/, T-cell depletion exacerbated listeriosis in ,-GalCer-treated mice, and this effect was more pronounced after depletion of Gr-1+ cells than that of ,/, T cells. Although GM-CSF and IL-17 were secreted by NKT cells after ,-GalCer treatment, liver infiltration of Gr-1+ cells was not prevented by neutralizing mAb. In parallel to the numerical increase of CD11b+Gr-1+ cells in the liver following ,-GalCer treatment, CD11b,Gr-1+ cells were numerically reduced in the bone marrow. In addition, respiratory burst in Gr-1+ cells was enhanced by ,-GalCer treatment. Our results indicate that ,-GalCer-induced antibacterial immunity is caused, in part, by accelerated infiltration of Gr-1+ cells and to a lesser degree of ,/, T cells into the liver. We also suggest that the infiltration of Gr-1+ cells is caused by an accelerated supply from the bone marrow. [source] Effector T-cell differentiation during viral and bacterial infections: Role of direct IL-12 signals for cell fate decision of CD8+ T cellsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2009Selina J. Keppler Abstract To study the role of IL-12 as a third signal for T-cell activation and differentiation in vivo, direct IL-12 signaling to CD8+ T cells was analyzed in bacterial and viral infections using the P14 T-cell adoptive transfer model with CD8+ T cells that lack the IL-12 receptor. Results indicate that CD8+ T cells deficient in IL-12 signaling were impaired in clonal expansion after Listeria monocytogenes infection but not after infection with lymphocytic choriomeningitis virus, vaccinia virus or vesicular stomatitis virus. Although limited in clonal expansion after Listeria infection, CD8+ T cells deficient in IL-12 signaling exhibited normal degranulation activity, cytolytic functions, and secretion of IFN-, and TNF-,. However, CD8+ T cells lacking IL-12 signaling failed to up-regulate KLRG1 and to down-regulate CD127 in the context of Listeria but not viral infections. Thus, direct IL-12 signaling to CD8+ T cells determines the cell fate decision between short-lived effector cells and memory precursor effector cells, which is dependent on pathogen-induced local cytokine milieu. [source] Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infectionFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 4 2000Tomisato Miura Abstract Various bacterial pathogens have been identified as mediators of apoptosis. Apoptosis reportedly shows both detrimental and beneficial effects on biological functions. We studied the role of liver apoptosis in lethal Listeria monocytogenes infection and the regulation of apoptosis by endogenous cytokines during infection. Apoptosis was observed in the spleen but not in the liver of infected mice, whereas the induction of liver necrosis was evident by rising levels of serum aminotransferases in these animals. Apoptosis was detected in the liver of L. monocytogenes -infected mice which had been treated with monoclonal antibody (mAb) against tumor necrosis factor-, (TNF-,) or interleukin-6 (IL-6), or in TNF-,,/, mice, but not in ,- interferon (IFN-,),/, mice or mice which had been treated with mAb against IL-4 or IL-10. Augmentation of liver apoptosis in mice treated with mAb against TNF-, or IL-6 or in TNF-,,/, mice correlated with the increase in bacterial numbers in the organ, while no augmentation of apoptosis was observed in the liver of IFN-,,/, mice irrespective of the marked increase in bacterial numbers in the organs, indicating that augmentation of liver apoptosis may not be merely due to the increase in bacterial growth in the organs. These results suggest that TNF-, and IL-6 may play an important role in protecting the liver from apoptosis in lethal L. monocytogenes infection. [source] Importance of murine V,1+,, T cells expressing interferon-, and interleukin-17A in innate protection against Listeria monocytogenes infectionIMMUNOLOGY, Issue 2 2008Satoru Hamada Summary Murine ,, T cells participate in the innate immune response against infection by an intracellular pathogen Listeria monocytogenes. V,1+,, T cells coexpressing V,6 are a major ,, T-cell subpopulation induced at an early stage of L. monocytogenes infection in the livers of infected mice. To investigate the protective role of the V,6/V,1+,, T cells against L. monocytogenes infection, V,1 gene-deficient (V,1,/,) mice were analysed because these mice selectively lacked a V,6/V,1+,, T-cell subpopulation in the L. monocytogenes -infected liver. The V,1,/, mice showed increased bacterial burden in the liver and spleen, and decreased survival rate at an early stage of L. monocytogenes infection when compared to wild-type mice. Histological examination showed abscess-like lesions and unorganized distribution of macrophages in the liver of the V,1,/, mice but not in the wild-type mice after L. monocytogenes infection. The V,6/V,1+,, T cells produced interferon-, and interleukin-17A. All the results suggest that murine V,6/V,1+,, T cells control the innate protective response against L. monocytogenes infection through production of the proinflammatory cytokines interferon-, and interleukin-17A in the infected liver. [source] Gastrointestinal phase of Listeria monocytogenes infectionJOURNAL OF APPLIED MICROBIOLOGY, Issue 6 2005C.G.M. Gahan [source] Modulation of hepatic cytochrome P450 during Listeria monocytogenes infection of the brainJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 9 2003Elena Garcia Del Busto Cano Abstract Hepatic cytochrome P450 enzymes can be modulated during systemic infections. Inflammatory responses in the brain have also been shown to cause a significant decrease in the levels and activities of important cytochrome P450 isoforms in the liver. We determined some of the effects of central nervous system (CNS) Listeria monocytogenes infection on hepatic cytochrome P450 systems in rats. Intracerebroventricular injection of L. monocytogenes resulted in a time-dependent modulation of CYP1A, CYP2B, and CYP3A activities in the liver. Total hepatic cytochrome P450 content was significantly lowered 48 h after administration of the bacterium, and hepatic CYP1A and CYP2B activities were significantly altered 48 and 72 h after infection, respectively, whereas CYP3A activity and protein content were depressed 72 h after the insult. Bacterial load in the brain increased dramatically over a 72-h period, but the number of bacteria cultured from liver over this time period was relatively small. Therefore, an infection largely confined to the CNS in the rat results in abnormal activity levels of certain hepatic cytochrome P450 enzymes crucial in drug metabolism. If such a response also occurs in humans, this has the potential to produce serious complications with drug and endogenous substrate metabolism in patients with an infectious disease involving the CNS. © 2003 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 92:1860,1868, 2003 [source] Report of an additional case of anti,tumor necrosis factor therapy and Listeria monocytogenes infection: Comment on the letter by Glück et alARTHRITIS & RHEUMATISM, Issue 6 2003Angel Garcia Aparicio MD No abstract is available for this article. [source] Listeria monocytogenes infection in the face of innate immunityCELLULAR MICROBIOLOGY, Issue 5 2009Sinead C. Corr Summary Pathogen recognition and induction of immune responses are important for efficient elimination of infection. However, pathogens such as Listeria monocytogenes employ strategies to evade or modulate these defences, thus creating a more favourable environment that ensures their survival and pathogenesis. New insights into these strategies, particularly those targeting innate immunity, have recently emerged. L. monocytogenes is initially detected at the cell surface or in phagosomes by toll-like receptor 2 and in the cytosol by nuclear oligodimerization domain (NOD)-like receptors (NOD1, NOD2) and NALP3 and Ipaf. It carries out N-deacetylation of peptidoglycan to avoid this detection by toll-like receptor 2 and NOD-like receptors. L. monocytogenes modulates transcription of host immunity genes through modification of histones and chromatin remodelling. Furthermore, L. monocytogenes has recently been shown to avoid autophagy and induce apoptosis in immune effector cells. In this review we discuss some of these strategies, which have provided new insights into the interaction between L. monocytogenes and the immune response at a crucial stage of infection. [source] | |||||||||||||