Disease relevance of Listeria

• The protective role of the perforin-dependent pathway has been shown for infection with the noncytopathic lymphocytic choriomeningitis virus, for infection with Listeria monocytogenes, and for the elimination of tumor cells by T cells and NK cells [1].
• In contrast to Listeria or Shigella, the actin-based motility of vaccinia is dependent on an unknown phosphotyrosine protein, but the underlying mechanism remains obscure [2].
• In addition, MSR-A-knockout mice show an increased susceptibility to infection with Listeria monocytogenes or herpes simplex virus type-1, indicating that MSR-A may play a part in host defence against pathogens [3].
• The combination of intrathecal gentamicin and a penicillin may be beneficial in refractory staphylococcal or Listeria meningitis [4].
• DAP12-deficient mice were more susceptible to endotoxic shock and had enhanced resistance to infection by the intracellular bacterium Listeria monocytogenes [5].

Psychiatry related information on Listeria

• The importance of intact host defense mechanisms for successful antimicrobial therapy was investigated via a comparison of the activities of ampicillin against experimental Listeria monocytogenes infections in normal mice and congenitally athymic (nude) mice [6].
• RESULTS: A patient with acute Listeria rhombencephalitis complained of formed musical auditory hallucinations on the side of recent sensorineural deafness [7].

High impact information on Listeria

• In the case of Listeria monocytogenes, the gene products responsible for virulence and for the introduction of antigens into the MHC class I pathway are being characterized [8].
• Structure of internalin, a major invasion protein of Listeria monocytogenes, in complex with its human receptor E-cadherin [9].
• InIB-dependent internalization of Listeria is mediated by the Met receptor tyrosine kinase [10].
• Eukaryotic expression vectors containing truncated genes of ActA and listeriolysin--two virulence factors of Listeria monocytogenes--have been used to transform S. typhimurium aroA [11].
• The association of Mena with the surface of the intracellular pathogen Listeria monocytogenes and the G-actin binding protein profilin suggests that this molecule may participate in bacterial movement by facilitating actin polymerization [12].

Chemical compound and disease context of Listeria

• The Listeria peptide is digested by carboxypeptidase Y but resists aminopeptidase M, and only peptides with N-formyl methionine competitively block its presentation to CTL [13].
• We treated a patient with staphylococcal meningitis refractory to methicillin sodium and oxacillin sodium, and a patient with Listeria meningitis refractory to penicillin G potassium and ampicillin sodium; both patients were cured when intrathecal gentamicin sulfate was added to the regimen [4].
• Two conditions produced increased secretion: (a) addition to the cultures of various agents that readily interacted with macrophages, such as latex particles, antibody-coated red cells, endotoxin, Listeria organisms, or Be salt; or (b) addition of activated lymphocytes [14].
• Tumor necrosis factor (TNF) is also a major player in the resolution of Listeria infections and is suggested to have more global effects than can be explained by the induction of IFN-gamma alone [15].
• These cells phagocytosed 5.7 mum diameter latex beads, rosetted with erythrocytes coated with IgG or with C3, killed Listeria monocytogenes, and synthesized both lysozyme and the second component of complement [16].

Biological context of Listeria

• Mice immunized with virulent Listeria monocytogenes generate CD8+ CTL with alpha beta receptors specific for a bacterial peptide presented by a conserved class I molecule encoded in the M region of the major histocompatibility complex [13].
• The inlA region was localized by transposon mutagenesis, cloned, and sequenced. inlA was introduced into Listeria innocua and shown to confer on this normally noninvasive species the ability to enter cells [17].
• Here, we show that tumor necrosis factor receptor p55-/- (TRp55-/-) mice are susceptible to Listeria monocytogenes infection in the presence of leukocyte recruitment, inflammatory cytokine production (including IFNgamma), nitric oxide synthesis, and oxidative burst formation [18].
• Mice of the H-2 d, H-2 b,and H-2 k haplotypes respond to this peptide upon infection with Listeria monocytogenes [19].
• InlB, a surface-localized protein of Listeria monocytogenes, induces phagocytosis in non-phagocytic mammalian cells by activating Met, a receptor tyrosine kinase [20].

Anatomical context of Listeria

• We report the identification of a previously unknown gene, inlA, which is necessary for the gram-positive intracellular pathogen Listeria monocytogenes to invade cultured epithelial cells [17].
• H-2M3 presents a Listeria monocytogenes peptide to cytotoxic T lymphocytes [13].
• Actin filament assembly at the cell surface of the pathogenic bacterium Listeria monocytogenes requires the bacterial ActA surface protein and the host cell Arp2/3 complex [21].
• We evaluated whether anti-LLO mAb would affect Listeria handling by macrophages, essential cells in Listeria resistance [22].
• We have identified a TNF/iNOS-producing (Tip)-DC subset in spleens of Listeria monocytogenes-infected mice that is absent from CCR2-deficient mice [23].

Gene context of Listeria

• Here we use flow cytometry to identify the presence of intracellular cytokines (cytoflow) and analyse T-cell production of IFN-gamma and IL-4 from mice infected with Listeria monocytogenes or Nippostrongylus brasiliensis [24].
• TCCR-deficient mice also had increased susceptibility to infection with an intracellular pathogen, Listeria monocytogenes [25].
• Here we show that Rip2-deficient mice exhibit a profoundly decreased ability to defend against infection by the intracellular pathogen Listeria monocytogenes [26].
• Infection with the intracellular bacterial pathogen Listeria monocytogenes induces CCR2-dependent monocyte recruitment and activation, an essential response for host survival [27].
• A critical role for interleukin 18 in primary and memory effector responses to Listeria monocytogenes that extends beyond its effects on Interferon gamma production [15].

Analytical, diagnostic and therapeutic context of Listeria

• Vaccination with heat-killed Listeria as adjuvant reverses established allergen-induced airway hyperreactivity and inflammation: role of CD8+ T cells and IL-18 [28].
• We analyzed the expression of the 47-kDa GTPase cognate, IIGP, in splenic sections from mice infected with the intracellular pathogen Listeria monocytogenes by immunohistochemistry [29].
• Our previous studies demonstrated that heat-killed Listeria monocytogenes (HKL) as an adjuvant in immunotherapy successfully reversed ongoing Ag-specific Th2-dominated responses toward Th1-dominated responses, but it was unclear if such immune modulation could reverse ongoing, established disease in target organs such as the lung [28].
• More recent studies have evaluated the efficacy of ciprofloxacin in animal models of tuberculosis and syphilis, as well as in infections caused by the intracellular pathogens Salmonella typhimurium, Legionella pneumophila, and Listeria monocytogenes [30].
• Immunosuppression has increased the incidence of central nervous system Listeria infections, but ampicillin still provides effective treatment, even when immunosuppressive therapy is continued [31].

References