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Berlin Brandenburg

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  • 1
    Language: English
    In: Journal of Infectious Diseases, June 15, 2010, Vol.201(12), p.S114(12)
    Keywords: Chlamydia Trachomatis -- Research ; Chlamydia Trachomatis -- Physiological Aspects ; Sexually Transmitted Diseases -- Research ; Sexually Transmitted Diseases -- Physiological Aspects ; T Cells -- Research ; T Cells -- Physiological Aspects ; Immune Response -- Research ; Immune Response -- Physiological Aspects
    ISSN: 0022-1899
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  • 2
    Language: English
    In: The Journal of Infectious Diseases, 15 June 2010, Vol.201, pp.S114-S125
    Description: Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s) that result in chlamydia-induced tissue damage are not fully understood. We reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infected nonimmune host epithelial cells. The mouse model indicates a critical role for chlamydia activation of the innate immune receptor, Toll-like receptor 2, and subsequent inflammatory cell influx and activation, which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-interferon-γ-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that, although the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis that thwart development of optimally effective control programs, including vaccine development.
    Keywords: Health sciences -- Medical conditions -- Infections -- Lymphocytes ; Biological sciences -- Biology -- Physiology -- Heterophils ; Biological sciences -- Biology -- Anatomy -- Heterophils ; Biological sciences -- Biology -- Anatomy -- Heterophils ; Biological sciences -- Biology -- Physiology -- Heterophils ; Biological sciences -- Biology -- Cytology -- Heterophils ; Biological sciences -- Biology -- Microbiology -- Heterophils ; Health sciences -- Medical specialties -- Pathology -- Heterophils ; Health sciences -- Medical specialties -- Pathology -- Heterophils ; Health sciences -- Medical conditions -- Diseases -- Heterophils
    ISSN: 00221899
    Source: Archival Journals (JSTOR)
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  • 3
    Language: English
    In: The Journal of Infectious Diseases, 15 June 2010, Vol.201, pp.S114-S125
    Description: Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s) that result in chlamydia-induced tissue damage are not fully understood. We reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infected nonimmune host epithelial cells. The mouse model indicates a critical role for chlamydia activation of the innate immune receptor, Toll-like receptor 2, and subsequent inflammatory cell influx and activation, which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-interferon-γ-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that, although the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis that thwart development of optimally effective control programs, including vaccine development.
    Keywords: Health sciences -- Medical conditions -- Infections -- Lymphocytes ; Biological sciences -- Biology -- Physiology -- Heterophils ; Biological sciences -- Biology -- Anatomy -- Heterophils ; Biological sciences -- Biology -- Anatomy -- Heterophils ; Biological sciences -- Biology -- Physiology -- Heterophils ; Biological sciences -- Biology -- Cytology -- Heterophils ; Biological sciences -- Biology -- Microbiology -- Heterophils ; Health sciences -- Medical specialties -- Pathology -- Heterophils ; Health sciences -- Medical specialties -- Pathology -- Heterophils ; Health sciences -- Medical conditions -- Diseases -- Heterophils
    ISSN: 00221899
    Source: Archival Journals (JSTOR)
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  • 4
    Language: English
    In: The Journal of Infectious Diseases, 06/15/2010, Vol.201(S2), pp.114-125
    Description: Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s)that result in chlamydia-induced tissue damage are not fully understood. We reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infected nonimmune host epithelial cells. The mouse model indicates a critical role for chlamydia activation of the innate immune receptor, Toll-like receptor 2, and subsequent inflammatory cell influx and activation, which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-interferon-g-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that, although the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis that thwart development of optimally effective control programs, including vaccine development.
    Keywords: Medicine ; Biology;
    ISSN: 0022-1899
    E-ISSN: 1537-6613
    Source: CrossRef
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  • 5
    Language: English
    In: The Journal of infectious diseases, 15 June 2010, Vol.201 Suppl 2, pp.S114-25
    Description: Although the pathologic consequences of C. trachomatis genital infection are well-established, the mechanism(s)that result in chlamydia-induced tissue damage are not fully understood. We reviewed in vitro, animal, and human data related to the pathogenesis of chlamydial disease to better understand how reproductive sequelae result from C. trachomatis infection. Abundant in vitro data suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infected nonimmune host epithelial cells. The mouse model indicates a critical role for chlamydia activation of the innate immune receptor, Toll-like receptor 2, and subsequent inflammatory cell influx and activation, which contributes to the development of chronic genital tract tissue damage. Data from recent vaccine studies in the murine model and from human immunoepidemiologic studies support a role for chlamydia-specific CD4 Th1-interferon-g-producing cells in protection from infection and disease. However, limited evidence obtained using animal models of repeated infection indicates that, although the adaptive T cell response is a key mechanism involved in controlling or eliminating infection, it may have a double-edged nature and contribute to tissue damage. Important immunologic questions include whether anamnestic CD4 T cell responses drive disease rather than protect against disease and the role of specific immune cells and inflammatory mediators in the induction of tissue damage with primary and repeated infections. Continued study of the complex molecular and cellular interactions between chlamydiae and their host and large-scale prospective immunoepidemiologic and immunopathologic studies are needed to address gaps in our understanding of pathogenesis that thwart development of optimally effective control programs, including vaccine development.
    Keywords: Chlamydia Infections -- Pathology ; Chlamydia Trachomatis -- Physiology
    E-ISSN: 1537-6613
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 6
    Language: English
    In: The Journal of infectious diseases, 01 March 2002, Vol.185(5), pp.627-31
    Description: Nontypeable Haemophilus influenzae (NTHI) is an important cause of lower respiratory tract infections in patients with chronic obstructive pulmonary disease. Recent findings suggest that the major outer membrane protein P2 should be reconsidered as a vaccine candidate for NTHI. A P2-based vaccine would require a relative degree of sequence stability of the gene encoding P2 (ompP2) during colonization. To characterize the sequence stability of ompP2 during colonization of the human respiratory tract, ompP2 genes from 13 sets of isolates that persisted in patients with chronic obstructive pulmonary disease (mean colonization, 7 months) were sequenced. In 9 sets of isolates, ompP2 did not change. Sequence changes were noted in 4 sets of isolates. Most of these changes occurred within areas of repetitive DNA, suggesting that this type of DNA has a role in antigenic variation of P2. The sequence of ompP2 is relatively stable during persistence of NTHI in the human host.
    Keywords: Bacterial Proteins ; Genetic Variation ; Sequence Analysis, DNA ; Bacterial Outer Membrane Proteins -- Genetics ; Haemophilus Influenzae -- Classification ; Porins -- Genetics ; Respiratory Tract Infections -- Microbiology
    ISSN: 0022-1899
    E-ISSN: 15376613
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  • 7
    Language: English
    In: The Journal of infectious diseases, 01 July 2003, Vol.188(1), pp.114-7
    Description: An adult with chronic obstructive pulmonary disease was monitored prospectively for 2 years. Nontypeable Haemophilus influenzae was isolated from sputum cultures at 22 of 23 monthly clinic visits. Analysis of the isolates, by pulsed-field gel electrophoresis (PFGE), revealed that the patient was colonized by 3 different strains during the 2-year period. The gene encoding outer-membrane protein (OMP) P2, ompP2, was amplified from sputum samples and selected strains obtained from this patient. Analysis of the ompP2 sequences, in combination with the PFGE patterns, indicated that ompP2 horizontal transfer between 2 strains occurred in the respiratory tract, between clinic visits 13 and 14. Observation of ompP2 horizontal transfer in the human respiratory tract has important implications for both the understanding of ompP2 diversity among strains and the future design of OMP P2-based vaccines.
    Keywords: Bacterial Outer Membrane Proteins -- Genetics ; Gene Transfer, Horizontal -- Genetics ; Haemophilus Infections -- Complications ; Haemophilus Influenzae -- Genetics ; Pulmonary Disease, Chronic Obstructive -- Complications
    ISSN: 0022-1899
    E-ISSN: 15376613
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  • 8
    In: Journal of Bacteriology, March, 1997, Vol.179(5-6), p.1764(10)
    Description: The nucleotide sequence of the gene encoding the major outer membrane protein (MOMP) of Haemophilus ducreyi was analyzed by sodium dodecyl sulfate-polyacrilamide gel electrophoresis. Nucleotide sequence analysis of the MOMP gene of Haemophilus ducreyi indicated the presence of two OmpA homologs that were encoded by momp and ompA2 genes. Southern blot analysis also indicated the high degree of similarity between MOMP and OmpA2 which existed in tandem in the different strains of Haemophilus ducreyi.
    Keywords: Pathogenic Bacteria -- Genetic Aspects ; Membrane Proteins -- Analysis ; Bacterial Proteins -- Analysis
    ISSN: 0021-9193
    E-ISSN: 10985530
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  • 9
    In: Infection and Immunity, 2000, Vol. 68(11), p.6250
    ISSN: 0019-9567
    ISSN: 00199567
    Source: American Society of Microbiology
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  • 10
    Language: English
    In: The Journal of Infectious Diseases, 1 June 1998, Vol.177(6), pp.1608-1613
    Description: Human subjects were infected with Haemophilus ducreyi. All subjects developed papules and were randomized to treatment with a single dose of azithromycin (1 g) or ciprofloxacin (500 mg). At weekly intervals, volunteers were reinoculated with H. ducreyi, and drug concentrations were measured in peripheral blood mononuclear cells (PBMC). When papules developed, the subjects were treated with antibiotics and dismissed from the study. Eight of the ciprofloxacin-treated subjects developed papules 1 week after the initial treatment, and the ninth subject developed disease 2 weeks after treatment. The 9 azithromycin-treated subjects developed papules 4-10 weeks (mean, 6.8) after the initial treatment (P 〈 .001). Azithromycin was detected in PBMC for 3-6 weeks (mean, 4). Pre-and posttreatment lesions had histology typical of experimental chancroid or were culture positive. Azithromycin prevents experimental chancroid for nearly 2 months. These findings have implications for strategies to prevent chancroid.
    Keywords: Health sciences -- Medical conditions -- Infections -- Haemophilus ducreyi ; Health sciences -- Medical sciences -- Pharmacology -- HIV ; Health sciences -- Medical conditions -- Infections -- HIV ; Health sciences -- Medical diagnosis -- Diagnostic methods -- HIV ; Biological sciences -- Biology -- Microbiology -- HIV ; Biological sciences -- Biology -- Microbiology -- HIV ; Biological sciences -- Biology -- Microbiology -- HIV ; Health sciences -- Medical specialties -- Pathology -- HIV ; Health sciences -- Medical conditions -- Physical trauma -- HIV ; Physical sciences -- Physics -- Microphysics -- HIV
    ISSN: 00221899
    E-ISSN: 15376613
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