Chlamydia pneumoniae as a respiratory pathogen

10.2741/hahn ◽  
2002 ◽  
Vol 7 (1-3) ◽  
pp. e66 ◽  
Author(s):  
David, L. Hahn
Keyword(s):  
Chlamydia Pneumoniae ◽  
Respiratory Pathogen

Anti-P. gingivalis Response Correlates with Atherosclerosis

2007 ◽  
Vol 86 (1) ◽  
pp. 35-40 ◽  
Author(s):  
P.J. Ford ◽  
E. Gemmell ◽  
P. Timms ◽  
A. Chan ◽  
F.M. Preston ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Chlamydia Pneumoniae ◽  
Molecular Mimicry ◽  
Respiratory Pathogen ◽  
Lesion Area ◽  
Lesion Development ◽  
Pathogen Burden ◽  
Antibody Levels ◽  
Deficient Mice

Significant associations between atherosclerosis and both Porphyromonas gingivalis, a major periodontopathogen, and the respiratory pathogen, Chlamydia pneumoniae, have been shown. Many individuals with evidence of atherosclerosis demonstrate seropositivity to these pathogens. The aim of the present study was to examine the atherogenic effect of repeated immunizations with either or both of these agents, and to determine if molecular mimicry of bacterial heat-shock protein (HSP), termed GroEL, and host (h) HSP60 was involved. Atherogenesis was examined in apolipoprotein-E-deficient (−/−) mice following intraperitoneal immunizations with P. gingivalis, C. pneumoniae, P. gingivalis, and C. pneumoniae or vehicle. Lesion area in the proximal aorta and levels of serum antibodies to P. gingivalis, C. pneumoniae, and GroEL were measured. The increased pathogen burden of P. gingivalis, but not of C. pneumoniae, enhanced atherosclerosis. hHSP60 was detected in lesions, and in P. gingivalis-immunized mice, lesion development was correlated with anti-GroEL antibody levels, supporting the involvement of molecular mimicry between GroEL and hHSP60.

scholarly journals Assaying Chlamydia pneumoniae persistence in monocyte-derived macrophages identifies schisandrin lignans as phenotypic switchers

2019 ◽  
Author(s):  
Eveliina Taavitsainen ◽  
Maarit Kortesoja ◽  
Leena Hanski
Keyword(s):  
Chlamydia Pneumoniae ◽  
Redox Status ◽  
Productive Infection ◽  
Respiratory Pathogen ◽  
Steady Increase ◽  
Intracellular Bacteria ◽  
Success Factor ◽  
Antibacterial Drug ◽  
Copy Numbers ◽  
Cell Redox Status

AbstractAntibiotic-tolerant persister bacteria involve frequent treatment failures, relapsing infections and the need for extended antibiotic treatment. Taking persisters into account in susceptibility assays is thus an essential success factor in antibacterial drug discovery. The virulence of the obligate intracellular bacterium Chlamydia pneumoniae is tightly linked to its propensity for persistence, but current susceptibility screening on this gram-negative respiratory pathogen relies on permissive epithelial cells. To establish an improved antichlamydial susceptibility assay allowing the analysis of both actively growing and persister bacteria, we studied C. pneumoniae clinical isolate CV-6 infection kinetics in THP-1 macrophages by qPCR and quantitative culture. Indicated by the steady increase of chlamydial genome copy numbers and infectious progeny as well as the failure of azithromycin to eradicate the intracellular forms of the bacterium, the macrophages were found to harbor a subpopulation of persister C. pneumoniae cells. The potential of the assay for the discovery of anti-persister molecules against intracellular bacteria was demonstrated by the identification of the differential effects of two dibenzocyclooctadiene lignans on C. pneumoniae infection. While schisandrin reverted C. pneumoniae persistence and promoted productive infection, schisandrin C was superior to azithromycin in eradicating the C. pneumoniae infection. The phenotypic switch was associated with the suppression of cellular glutathione pools, implying that targeting glutathione homeostasis may provide a novel means for intracellular bacteria resuscitation. In conclusion, these data highlight the value of macrophages over permissive cell lines in anti-persister agent discovery on intracellular bacteria and targeting host cell redox status to fight persistent infections.

scholarly journals Chlamydia pneumoniae and chronic asthma: Updated systematic review and meta-analysis of population attributable risk

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250034
Author(s):  
David L. Hahn
Keyword(s):  
Chlamydia Pneumoniae ◽  
Population Attributable Risk ◽  
Asthma Severity ◽  
Specific Ige ◽  
Attributable Risk ◽  
Respiratory Pathogen ◽  
Chronic Asthma ◽  
Case Control Studies ◽  
Specific Igg ◽  
Population Attributable Risks

Background Chlamydia pneumoniae (Cp) is an obligate intracellular human respiratory pathogen producing persisting lung infection with a plausible link to asthma pathogenesis. The population attributable risk of potentially treatable Cp infection in asthma has not been reported. Methods The author searched from 2000 to 2020 inclusive for previously un-reviewed and new cross sectional and prospective controlled studies of Cp biomarkers and chronic asthma in both children and adults. Qualitative descriptive results and quantitative estimates of population attributable risk for selected biomarkers (specific IgG, IgA and IgE) are presented. Findings No large, long-term prospective population-based studies of Cp infection and asthma were identified. About half of case-control studies reported one or more significant associations of Cp biomarkers and chronic asthma. Heterogeneity of results by age group (pediatric v adult asthma), severity category (severe/uncontrolled, moderate/partly controlled, mild/controlled) and antibody isotype (specific IgG, IgA, IgE) were suggested by the qualitative results and confirmed by meta-analyses. The population attributable risks for Cp-specific IgG and IgA were nul in children and were 6% (95% confidence interval 2%-10%, p = 0.002) and 13% (9%-18%, p<0.00001) respectively in adults. In contrast to the nul or small population attributable risks for Cp-specific IgG and IgA, the population attributable risk for C. pneumoniae-specific IgE (children and adults combined) was 47% (39%-55%, p<0.00001). In the subset of studies that reported on asthma severity categories, Cp biomarkers were positively and significantly (P<0.00001) associated with asthma severity. Interpretation C. pneumoniae-specific IgE is strongly associated with asthma and asthma severity, suggesting a possible mechanism linking chronic Cp infection with asthma in a subset of individuals with asthma. Infection biomarkers should be included in future macrolide treatment trials for severe and uncontrolled asthma.

scholarly journals Failure To Detect Chlamydia pneumoniaein the Late-Onset Alzheimer's Brain

2000 ◽  
Vol 38 (7) ◽  
pp. 2591-2594 ◽  
Author(s):  
Robert H. Ring ◽  
Joseph M. Lyons
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Chlamydia Pneumoniae ◽  
Late Onset ◽  
Brain Regions ◽  
Postmortem Brain ◽  
Respiratory Pathogen ◽  
Specific Gene ◽  
Tissue Samples ◽  
Postmortem Brain Tissue

Epidemiological studies have yet to identify a single cause for the most common late-onset form of Alzheimer's disease. The common respiratory pathogen Chlamydia pneumoniae recently has been implicated as a risk factor for this form of Alzheimer's disease. Were this true, there would be a dramatic shift in current paradigms of Alzheimer's disease research and treatment. In the absence of published confirmation, we obtained postmortem brain tissue from late-onset Alzheimer's disease patients (n = 15) and representative controls (n = 5) and extracted DNA from up to six separate brain regions in each instance, including those areas particularly relevant to Alzheimer's disease neuropathology. Each sample of DNA (n = 101) was assayed five times or more for the presence of C. pneumoniae DNA using a nested-PCR protocol targeting a species-specific gene sequence coding for the major outer membrane protein of this organism. We were unable unequivocally to detect C. pneumoniae in any of the 101 samples tested by PCR and failed to culture the organism from tissue samples. We conclude that C. pneumoniae is neither strongly nor uniquely associated with the neuropathology seen in late-onset Alzheimer's disease.

scholarly journals Detection of Chlamydia pneumoniae DNA and Antigen in the Circulating Mononuclear Cell Fractions of Humans and Koalas

2000 ◽  
Vol 68 (5) ◽  
pp. 2744-2747 ◽  
Author(s):  
Tracey J. Bodetti ◽  
Peter Timms
Keyword(s):  
Mononuclear Cell ◽  
Blood Donors ◽  
Chlamydia Pneumoniae ◽  
Respiratory Infections ◽  
General Characteristic ◽  
Respiratory Pathogen ◽  
Healthy Human ◽  
Specific Staining ◽  
Peripheral Blood Mononuclear ◽  
Antibody Staining

ABSTRACT Chlamydia pneumoniae is a common respiratory pathogen of humans which, in addition to causing disease at the respiratory site, has recently been linked to disease at other body sites. IfC. pneumoniae does contribute to disease at nonrespiratory sites, then it must have a mechanism by which it reaches these sites. We analyzed the peripheral blood mononuclear cell (PBMC) fractions from 60 healthy human blood donors for the presence of C. pneumoniae DNA (by ompA PCR) and chlamydial antigens (by genus- and species-specific monoclonal antibody staining). Ten of the sixty (16.7%) blood donors were C. pneumoniae positive by PCR, and all 10 of these PCR-positive individuals' samples demonstrated specific staining with anti-C. pneumoniaemonoclonal antibodies. The only other host naturally infected withC. pneumoniae is the koala, in which the bacterium also causes respiratory infections. We demonstrated the presence of C. pneumoniae DNA and antigens in the PBMC fractions of 30% of 20 koalas tested. Our finding of C. pneumoniae-infected PBMCs in koalas as well as humans suggests that the ability to infect PBMCs and to disseminate from the respiratory site is not restricted to the human biovar of C. pneumoniae but is a general characteristic of this chlamydial species.

scholarly journals Proteomic Analysis of Differentially Expressed Chlamydia pneumoniae Genes during Persistent Infection of HEp-2 Cells

2002 ◽  
Vol 70 (6) ◽  
pp. 2976-2981 ◽  
Author(s):  
Robert E. Molestina ◽  
Jon B. Klein ◽  
Richard D. Miller ◽  
William H. Pierce ◽  
Julio A. Ramirez ◽  
...  
Keyword(s):  
Persistent Infection ◽  
Chlamydia Pneumoniae ◽  
Differentially Expressed ◽  
Respiratory Pathogen ◽  
Developmental Cycle ◽  
Ionization Mass ◽  
Heat Shock Protein 60 ◽  
Ifn Γ ◽  
Gene Transcription Profile

ABSTRACT Recent data have shown that the respiratory pathogen Chlamydia pneumoniae expresses an altered gene transcription profile during gamma interferon (IFN-γ)-induced persistent infection in vitro. In the present study, we examined, by proteomics, expression of C. pneumoniae proteins labeled intracellularly with [35S]methionine/cysteine under normal conditions or IFN-γ-mediated persistence. The identity of differentially expressed proteins during persistent infection was determined by matching spots to those of proteins identified in C. pneumoniae elementary bodies by matrix-assisted laser desorption ionization mass spectrometry. Upon treatment with 50 U of IFN-γ per ml, a marked upregulation of major outer membrane protein (MOMP), heat shock protein 60 (Hsp-60/GroEL), and proteins with functions in DNA replication (GyrA), transcription (RpoA, PnP), translation (Rrf), glycolysis (PgK, GlgP), and type III secretion (SctN) was observed at 24 h of infection. In contrast, no significant decreases in bacterial protein expression were found in C. pneumoniae-infected cells due to IFN-γ treatment. Upregulation of C. pneumoniae proteins involved in diverse functions during persistent infection may allow the organism to resist the inhibitory effects of IFN-γ while retaining basic functions. Future studies should examine the differential expression of chlamydial proteins during the developmental cycle under IFN-γ pressure to obtain a finer representation of the gene products involved in establishing persistence.

Multiple genotypes of Chlamydia pneumoniae identified in human carotid plaque

Microbiology ◽  
2005 ◽  
Vol 151 (7) ◽  
pp. 2285-2290 ◽  
Author(s):  
Melanie Cochrane ◽  
Philip Walker ◽  
Harry Gibbs ◽  
Peter Timms
Keyword(s):  
Carotid Plaque ◽  
Chlamydia Pneumoniae ◽  
Protein A ◽  
Genomic Analysis ◽  
Community Acquired Pneumonia ◽  
Respiratory Pathogen ◽  
Specific Gene ◽  
Obligate Intracellular ◽  
Outer Membrane Protein A ◽  
Human Carotid

Chlamydia pneumoniae is an obligate intracellular respiratory pathogen that causes 10 % of community-acquired pneumonia and has been associated with cardiovascular disease. Both whole-genome sequencing and specific gene typing suggest that there is relatively little genetic variation in human isolates of C. pneumoniae. To date, there has been little genomic analysis of strains from human cardiovascular sites. The genotypes of C. pneumoniae present in human atherosclerotic carotid plaque were analysed and several polymorphisms in the variable domain 4 (VD4) region of the outer-membrane protein-A (ompA) gene and the intergenic region between the ygeD and uridine kinase (ygeD–urk) genes were found. While one genotype was identified that was the same as one reported previously in humans (respiratory and cardiovascular), another genotype was found that was identical to a genotype from non-human sources (frog/koala).

scholarly journals De Novo Induction of Atherosclerosis byChlamydia pneumoniae in a Rabbit Model

1999 ◽  
Vol 67 (11) ◽  
pp. 6048-6055 ◽  
Author(s):  
Ignatius W. Fong ◽  
Brian Chiu ◽  
Esther Viira ◽  
Dan Jang ◽  
James B. Mahony
Keyword(s):  
Chlamydia Pneumoniae ◽  
De Novo ◽  
Rabbit Model ◽  
Tissue Growth ◽  
Respiratory Pathogen ◽  
Cholesterol Diet ◽  
Histological Changes ◽  
Tract Pathogen ◽  
Induced Changes ◽  
Grade Iii

ABSTRACT Chlamydia pneumoniae, a bacterial respiratory tract pathogen, has been associated with atherosclerosis in humans. C. pneumoniae infection of the respiratory tracts of rabbits fed a noncholesterol diet induced changes of atherosclerosis of the aorta in 6 (26.1%) of 23 animals after a single inoculum at 3 months. Multiple inocula given three times within 6 weeks resulted in grade III atherosclerosis in 8 (34.8%) of 23 rabbits, with an additional 5 (21.7%) showing increased myxoid changes in the intima-media junction and exhibiting 8 (34.8%) focal periaortitis. Control animals inoculated with carrier broth (n = 24), HEp-2 cells (n = 12), or another respiratory pathogen,Mycoplasma pneumoniae (n = 32), produced no changes of atherosclerosis after 3 months. The histological changes were dissimilar (fewer foam cells) from those of rabbits fed a 0.5% cholesterol diet but were highly similar to or indistinguishable from changes in rabbits fed a 0.15% cholesterol diet (similar to that of humans). Proinflammatory cytokines and tissue growth factors were more consistently detected in cholesterol-induced aortic lesions than those induced by C. pneumoniae. These data are compatible with de novo induction of atherogenesis by C. pneumoniae in rabbits and suggest that C. pneumoniae may be important in the pathogenesis of atherosclerosis in humans.

Sign in / Sign up

Export Citation Format

Share Document