about
Chlamydia trachomatis Genital Infections.Steroids alone or as adjunctive therapy with doxycycline fail to improve oviduct damage in mice infected with Chlamydia muridarum.Enhanced virulence of Chlamydia muridarum respiratory infections in the absence of TLR2 activation.Plasmid-cured Chlamydia caviae activates TLR2-dependent signaling and retains virulence in the guinea pig model of genital tract infection.Infectivity acts as in vivo selection for maintenance of the chlamydial cryptic plasmidToll-like receptor 2 activation by Chlamydia trachomatis is plasmid dependent, and plasmid-responsive chromosomal loci are coordinately regulated in response to glucose limitation by C. trachomatis but not by C. muridarumChlamydial infection increases gonococcal colonization in a novel murine coinfection model.Enhanced neutrophil longevity and recruitment contribute to the severity of oviduct pathology during Chlamydia muridarum infection.Frequency of Chlamydia trachomatis-specific T cell interferon-γ and interleukin-17 responses in CD4-enriched peripheral blood mononuclear cells of sexually active adolescent females.The recall response induced by genital challenge with Chlamydia muridarum protects the oviduct from pathology but not from reinfectionComparable Genital Tract Infection, Pathology, and Immunity in Rhesus Macaques Inoculated with Wild-Type or Plasmid-Deficient Chlamydia trachomatis Serovar DBinding of C4b-binding protein to porin: a molecular mechanism of serum resistance of Neisseria gonorrhoeae.Analysis of Factors Driving Incident and Ascending Infection and the Role of Serum Antibody in Chlamydia trachomatis Genital Tract Infection.Identification of Chlamydia trachomatis Antigens Recognized by T Cells From Highly Exposed Women Who Limit or Resist Genital Tract Infection.A plasmid-cured Chlamydia muridarum strain displays altered plaque morphology and reduced infectivity in cell culture.Localization of TLR2 and MyD88 to Chlamydia trachomatis inclusions. Evidence for signaling by intracellular TLR2 during infection with an obligate intracellular pathogen.A Chlamydia-Specific TCR-Transgenic Mouse Demonstrates Th1 Polyfunctionality with Enhanced Effector Function.Whole-Exome Sequencing to Identify Novel Biological Pathways Associated With Infertility After Pelvic Inflammatory Disease.Risk factors for Mycoplasma genitalium endometritis and incident infection: a secondary data analysis of the T cell Response Against Chlamydia (TRAC) Study.T-independent IFNγ and B cells Cooperate to Prevent Mortality Associated with Disseminated Chlamydia muridarum Genital Tract Infection.Discovery of Blood Transcriptional Endotypes in Women with Pelvic Inflammatory Disease.Gene Expression Signatures Can Aid Diagnosis of Sexually Transmitted Infection-Induced Endometritis in WomenSimultaneous profiling of sexually transmitted bacterial pathogens, microbiome, and concordant host response in cervical samples using whole transcriptome sequencing analysisDiscovery of Human-Specific Immunodominant Chlamydia trachomatis B Cell EpitopesComprehensive Molecular Serology of Human Chlamydia trachomatis Infections by Peptide Enzyme-Linked Immunosorbent AssaysAnti-chlamydia IgG and IgA are insufficient to prevent endometrial chlamydia infection in women, and increased anti-chlamydia IgG is associated with enhanced risk for incident infectionCervical Cytokines Associated With Chlamydia trachomatis Susceptibility and Protection
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Catherine M O'Connell
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Catherine M O'Connell
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Catherine M O'Connell
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Catherine M O'Connell
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Catherine M O'Connell
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Catherine M O'Connell
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Catherine M O'Connell
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