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  • American Society for Microbiology  (35)
  • Meyer, Thomas F.  (35)
  • 1
    Online Resource
    Online Resource
    Roles of PilC and PilE Proteins in Pilus-Mediated Adherence of Neisseria gonorrhoeae and Neisseria meningitidis to Human Erythrocytes and Endothelial and Epithelial Cells
    American Society for Microbiology ; 1999
    In:  Infection and Immunity Vol. 67, No. 2 ( 1999-02), p. 834-843
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 67, No. 2 ( 1999-02), p. 834-843
    Abstract: Unlike other type 4 pili, the neisserial pili consist of at least two distinct proteins, the highly variable major subunit PilE forming the pilus fiber and the tip-associated adhesin PilC. PilC protein purified either from gonococci or from Escherichia coli interacted with different human epithelial cell lines, primary epithelial and endothelial cells. The binding of PilC protein efficiently prevented the attachment of piliated Neisseria gonorrhoeae and Neisseria meningitidis to these cell types. Fluorescent beads coated with pili prepared from piliated wild-type N. gonorrhoeae also adhered to these cells, in contrast to beads coated with pili prepared from a piliated PilC-deficient mutant. In the latter case, the binding of fluorescent beads was restored after pretreatment of the pilus-loaded beads with purified PilC. Piliated wild-type N. gonorrhoeae , the piliated PilC-deficient mutant, and N. gonorrhoeae pili assembled in Pseudomonas aeruginosa agglutinated human erythrocytes, while nonpiliated gonococci did not. Consistently, purified PilC did not agglutinate or bind to human erythrocytes, suggesting that N. gonorrhoeae PilE is responsible for pilus-mediated hemagglutination.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.67.2.834-843.1999
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
    detail.hit.zdb_id: 1483247-1
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  • 2
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    Low-Phosphate-Dependent Invasion Resembles a General Way for Neisseria gonorrhoeae To Enter Host Cells
    American Society for Microbiology ; 2006
    In:  Infection and Immunity Vol. 74, No. 7 ( 2006-07), p. 4266-4273
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 74, No. 7 ( 2006-07), p. 4266-4273
    Abstract: Obligate human-pathogenic Neisseria gonorrhoeae expresses numerous variant surface proteins mediating adherence to and invasion of target cells. The invariant major outer membrane porin PorB of serotype A (P.IA) gonococci triggers invasion into Chang cells only if the medium is devoid of phosphate. Since gonococci expressing PorB IA are frequently isolated from patients with severe disseminating infections, the interaction initiated by the porin may be of major relevance for the development of this serious disease. Here, we investigated the low-phosphate-dependent invasion and compared it to the well-known pathways of entry initiated by Opa proteins. P.IA-triggered invasion requires clathrin-coated pit formation and the action of actin and Rho GTPases. However, in contrast to Opa-initiated invasion via heparan sulfate proteoglycans, microtubules, acidic sphingomyelinase, phosphatidylinositol 3-kinase, and myosin light chain kinase are not involved in this entry pathway. Nor are Src kinases required, as they are in invasion, e.g., via the CEACAM3 receptor. Invasion by PorB IA occurs in a wide spectrum of cell types, such as primary human epithelial and endothelial cells and in cancer cells of human and animal origin. Low-phosphate-dependent invasion is thus a pathway of gonococcal entry distinct from Opa-mediated invasion.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00215-06
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2006
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  • 3
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    Neisseria gonorrhoeae Porin Modifies the Oxidative Burst of Human Professional Phagocytes
    American Society for Microbiology ; 2000
    In:  Infection and Immunity Vol. 68, No. 11 ( 2000), p. 6215-6222
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 68, No. 11 ( 2000), p. 6215-6222
    Type of Medium: Online Resource
    ISSN: 1098-5522 , 0019-9567
    URL: Article
    DOI: 10.1128/.68.11.6215-6222.2000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2000
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  • 4
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    Epithelial Cells Infected with Chlamydophila pneumoniae ( Chlamydia pneumoniae ) Are Resistant to Apoptosis
    American Society for Microbiology ; 2001
    In:  Infection and Immunity Vol. 69, No. 12 ( 2001-12), p. 7880-7888
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 69, No. 12 ( 2001-12), p. 7880-7888
    Abstract: The obligate intracellular pathogen Chlamydophila pneumoniae ( Chlamydia pneumoniae ) initiates infections in humans via the mucosal epithelia of the respiratory tract. Here, we report that epithelial cells infected with C. pneumoniae are resistant to apoptosis induced by treatment with drugs or by death receptor ligation. The induction of protection from apoptosis depended on the infection conditions since only cells containing large inclusions were protected. The underlying mechanism of infection-induced apoptosis resistance probably involves mitochondria, the major integrators of apoptotic signaling. In the infected cells, mitochondria did not respond to apoptotic stimuli by the release of apoptogenic factors required for the activation of caspases. Consequently, active caspase-3 was absent in infected cells. Our data suggest a direct modulation of apoptotic pathways in epithelial cells by C. pneumoniae .
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.69.12.7880-7888.2001
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 5
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    Neisseria gonorrhoeae Porin Modifies the Oxidative Burst of Human Professional Phagocytes
    American Society for Microbiology ; 2000
    In:  Infection and Immunity Vol. 68, No. 11 ( 2000-11), p. 6215-6222
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 68, No. 11 ( 2000-11), p. 6215-6222
    Abstract: A hallmark of infection with the gram-negative bacterium Neisseria gonorrhoeae is the local infiltration and subsequent activation of polymorphonuclear neutrophils. Several gonococcal outer membrane proteins are involved in the interaction with and the activation of these phagocytes, including gonococcal porin, the most abundant protein in the outer membrane. Previous work suggests that this porin plays a role in various cellular processes, including inhibiting neutrophils activation and phagosome maturation in professional phagocytes. Here we investigated the ability of porin to modify the oxidative metabolism of human peripheral blood neutrophils and monocytes in response to particulate stimuli (including live gonococci) and soluble agents. The activation of the oxidative metabolism was determined by chemiluminescence amplified with either luminol or lucigenin. We found that treatment of the phagocytes with porin inhibits the release of reactive oxygen species measured as luminol-enhanced chemiluminescence in response to zymosan, latex particles, and gonococci. The engulfment of these particles was not, however, affected by porin treatment. Similar effects of porin on the chemiluminescence response were observed in cytochalasin B-treated neutrophils exposed to the soluble chemotactic peptide N -formylmethionyl-leucyl-phenylalanine. This indicates that porin selectively inhibits granule fusion with those cellular membranes that are in direct contact with porin, namely, the phagosomal and plasma membranes. This porin-induced downregulation of oxidative metabolism may be a potent mechanism by which gonococci modulate oxygen-dependent reactions by activated phagocytes at inflammation sites.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.68.11.6215-6222.2000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2000
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  • 6
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    Comparative Analysis of the Interaction of Helicobacter pylori with Human Dendritic Cells, Macrophages, and Monocytes
    American Society for Microbiology ; 2012
    In:  Infection and Immunity Vol. 80, No. 8 ( 2012-08), p. 2724-2734
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 80, No. 8 ( 2012-08), p. 2724-2734
    Abstract: Helicobacter pylori may cause chronic gastritis, gastric cancer, or lymphoma. Myeloid antigen-presenting cells (APCs) are most likely involved in the induction and expression of the underlying inflammatory responses. To study the interaction of human APC subsets with H. pylori , we infected monocytes, monocyte-derived dendritic cells (DCs), and monocyte-derived (classically activated; M1) macrophages with H. pylori and analyzed phenotypic alterations, cytokine secretion, phagocytosis, and immunostimulation. Since we detected CD163 + (alternatively activated; M2) macrophages in gastric biopsy specimens from H. pylori -positive patients, we also included monocyte-derived M2 macrophages in the study. Upon H. pylori infection, monocytes secreted interleukin-1β (IL-1β), IL-6, IL-10, and IL-12p40 (partially secreted as IL-23) but not IL-12p70. Infected DCs became activated, as shown by the enhanced expression of CD25, CD80, CD83, PDL-1, and CCR7, and secreted IL-1β, IL-6, IL-10, IL-12p40, IL-12p70, and IL-23. However, infection led to significantly downregulated CD209 and suppressed the constitutive secretion of macrophage migration inhibitory factor (MIF). H. pylori -infected M1 macrophages upregulated CD14 and CD32, downregulated CD11b and HLA-DR, and secreted mainly IL-1β, IL-6, IL-10, IL-12p40, and IL-23. Activation of DCs and M1 macrophages correlated with increased capacity to induce T-cell proliferation and decreased phagocytosis of dextran. M2 macrophages upregulated CD14 and CD206 and secreted IL-10 but produced less of the proinflammatory cytokines than M1 macrophages. Thus, H. pylori affects the functions of human APC subsets differently, which may influence the course and the outcome of H. pylori infection. The suppression of MIF in DCs constitutes a novel immune evasion mechanism exploited by H. pylori .
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.00381-12
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2012
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  • 7
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    Modulation of Host Cell Metabolism by Chlamydia trachomatis
    American Society for Microbiology ; 2019
    In:  Microbiology Spectrum Vol. 7, No. 3 ( 2019-05-31)
    Details
    In: Microbiology Spectrum, American Society for Microbiology, Vol. 7, No. 3 ( 2019-05-31)
    Abstract: Propagation of the intracellular bacterial pathogen Chlamydia trachomatis is strictly bound to its host cells. The bacterium has evolved by minimizing its genome size at the cost of being completely dependent on its host. Many of the vital nutrients are synthesized only by the host, and this has complex implications. Recent advances in loss-of-function analyses and the metabolomics of human infected versus noninfected cells have provided comprehensive insight into the molecular changes that host cells undergo during the stage of infection. Strikingly, infected cells acquire a stage of high metabolic activity, featuring distinct aspects of the Warburg effect, a condition originally assigned to cancer cells. This condition is characterized by aerobic glycolysis and an accumulation of certain metabolites, altogether promoting the synthesis of crucial cellular building blocks, such as nucleotides required for DNA and RNA synthesis. The altered metabolic program enables tumor cells to rapidly proliferate as well as C. trachomatis -infected cells to feed their occupants and still survive. This program is largely orchestrated by a central control board, the tumor suppressor protein p53. Its downregulation in C. trachomatis -infected cells or mutation in cancer cells not only alters the metabolic state of cells but also conveys the prevention of programmed cell death involving mitochondrial pathways. While this points toward common features in the metabolic reprogramming of infected and rapidly proliferating cells, it also forwards novel treatment options against chronic intracellular infections involving well-characterized host cell targets and established drugs.
    Type of Medium: Online Resource
    ISSN: 2165-0497
    URL: Article
    DOI: 10.1128/microbiolspec.BAI-0012-2019
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2019
    detail.hit.zdb_id: 2807133-5
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  • 8
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    Functional Analysis of the cag Pathogenicity Island in Helicobacter pylori Isolates from Patients with Gastritis, Peptic Ulcer, and Gastric Cancer
    American Society for Microbiology ; 2004
    In:  Infection and Immunity Vol. 72, No. 2 ( 2004-02), p. 1043-1056
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 72, No. 2 ( 2004-02), p. 1043-1056
    Abstract: Helicobacter pylori is the causative agent of a variety of gastric diseases, but the clinical relevance of bacterial virulence factors is still controversial. Virulent strains carrying the cag pathogenicity island ( cag PAI) are thought to be key players in disease development. Here, we have compared cag PAI-dependent in vitro responses in H. pylori isolates obtained from 75 patients with gastritis, peptic ulcer, and gastric cancer ( n = 25 in each group). AGS gastric epithelial cells were infected with each strain and assayed for (i) CagA expression, (ii) translocation and tyrosine phosphorylation of CagA, (iii) c-Src inactivation, (iv) cortactin dephosphorylation, (v) induction of actin cytoskeletal rearrangements associated with cell elongation, (vi) induction of cellular motility, and (vii) secretion of interleukin-8. Interestingly, we found high but similar prevalences of all of these cag PAI-dependent host cell responses (ranging from 56 to 80%) among the various groups of patients. This study revealed CagA proteins with unique features, CagA subspecies of various sizes, and new functional properties for the phenotypic outcomes. We further showed that induction of AGS cell motility and elongation are two independent processes. Our data corroborate epidemiological studies, which indicate a significant association of cag PAI presence and functionality with histopathological findings in gastritis, peptic ulcer, and gastric cancer patients, thus emphasizing the importance of the cag PAI for the pathogenicity of H. pylori . Nevertheless, we found no significant association of the specific H. pylori -induced responses with any particular patient group. This may indicate that the determination of disease development is highly complex and involves multiple bacterial and/or host factors.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.72.2.1043-1056.2004
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2004
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  • 9
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    Tyrosine Phosphatase SHP-1 Is Involved in CD66-Mediated Phagocytosis of Opa 52 -Expressing Neisseria gonorrhoeae
    American Society for Microbiology ; 1999
    In:  Infection and Immunity Vol. 67, No. 10 ( 1999-10), p. 5490-5494
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 67, No. 10 ( 1999-10), p. 5490-5494
    Abstract: Opa proteins of Neisseria gonorrhoeae bind to CD66 receptors on human phagocytes, thereby inducing efficient uptake of the bacteria in the absence of opsonins. The interaction of Opa proteins and CD66 receptors leads to activation of Src family tyrosine kinases, a process that is of critical importance for the efficient, CD66-mediated internalization. Here we show that during Opa-mediated stimulation of CD66 the activity of the host cell tyrosine phosphatase SHP-1 is strongly downregulated, concomitant with increases in the tyrosine phosphorylation of several cellular proteins. Since the SHP-1 tyrosine phosphorylation level itself is influenced by Opa-induced events, this phosphatase comprises an important regulatory checkpoint of the pathogen-triggered signaling cascade in human phagocytes.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.67.10.5490-5494.1999
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
    detail.hit.zdb_id: 1483247-1
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  • 10
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    Helicobacter pylori Induces AGS Cell Motility and Elongation via Independent Signaling Pathways
    American Society for Microbiology ; 2004
    In:  Infection and Immunity Vol. 72, No. 6 ( 2004-06), p. 3646-3649
    Details
    In: Infection and Immunity, American Society for Microbiology, Vol. 72, No. 6 ( 2004-06), p. 3646-3649
    Abstract: Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    URL: Article
    DOI: 10.1128/IAI.72.6.3646-3649.2004
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2004
    detail.hit.zdb_id: 1483247-1
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