Experimental infection with Chlamydia pneumoniae in nonhuman primates

Holland, Steven M.; Taylor, Hugh R.; Gaydos, Charlotte A.; Kappus, Elizabeth W.; Quinn, Thomas C.

doi:10.1128/iai.58.3.593-597.1990

Cited by 27 publications

(9 citation statements)

References 11 publications

(15 reference statements)

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“…Frozen aliquots of respiratory specimens from two cynomolgus monkeys that were experimentally inoculated with C. pneumoniae were also available for testing (17). Specimens were obtained from nostrils and nasopharynxes both before and after inoculation.…”

Section: Resultsmentioning

confidence: 99%

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Identification of Chlamydia pneumoniae by DNA amplification of the 16S rRNA gene

1992

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Chlamydia pneumoniae is an important cause of respiratory disease in humans, but diagnosis of C. pneumoniae is hindered by difficulties in the in vitro growth of the organism. In order to improve detection and identification, we recently developed a polymerase chain reaction (PCR) assay which uses oligonucleotide primers specific for C. pneumoniae. The nucleic acid sequence was determined for the 16S rRNA of C. pneumoniae, and regions in which C. pneumoniae differed from both Chlamydia psittaci and Chlamydia trachomatis were identified. Oligonucleotide primers corresponding to these unique regions were then synthesized and used in a PCR for the detection of C. pneumoniae. The C. pneumoniae-specific primers permitted the identification of six isolates of C. pneunwniae, but no reaction was observed with the 15 serovars of C. trachomatis or two strains of C. psittaci. PCR should prove to be valuable in confirming the identification of C. pneumoniae and in the diagnosis of C. pneumoniae infections.

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Section: Resultsmentioning

confidence: 99%

“…Two specimens were obtained from each monkey prior to inoculation with C. pneumoniae; and 12 specimens were obtained at weeks 1, 4, and 18 post-inoculation (p.i.). A reinoculation occurred at week 15 (17). For these clinical specimens, PCR products were detected by PCR-enzyme immunoassay (3).…”

Section: Materuils and Methodsmentioning

confidence: 99%

Identification of Chlamydia pneumoniae by DNA amplification of the 16S rRNA gene

1992

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“…In the nonhuman primate models (baboons and cynomolgus monkeys), mild or asymptomatic chronic respiratory tract infection (mild interstitial pneumonia) developed after intranasal inoculation (1,8). Recently, Moazed et al (18) has described C. pneumoniae infections of the rabbit.…”

Section: Discussionmentioning

confidence: 99%

Rabbit model for Chlamydia pneumoniae infection

et al. 1997

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A rabbit model was established for Chlamydia pneumoniae infection that may be helpful to understand the pathogenesis of disease in humans. Twelve, pathogen-free, 1-month-old New Zealand White rabbits were inoculated with 1.0 ؋ 10 7 to 5.0 ؋ 10 7 CFU of purified C. pneumoniae (ATCC strain VR 1310) via the nasopharynx (1 rabbit died immediately postinoculation, and 11 were available for study). Five controls were inoculated with the carrier buffer. Ten of the 11 study rabbits demonstrated serological evidence of acute infection (immunoglobulin G antibodies, 1:8 to >1:16), with the weakest response at 7 days and the strongest response at 28 days, whereas none of the controls showed any seroconversion. Study animals were sacrificed in batches of three, on days 7, 14, 21, and 28, but controls were sacrificed on days 7 and 28. Two-thirds of the animals demonstrated evidence of bronchiolitis and pneumonia on days 7 and 14 and resolution by day 21. Two study rabbits demonstrated, on histology, early and intermediate lesions of atherosclerosis: one animal (day 7) showed the accumulation of foamy macrophages (fatty streak) in the arch of the aorta, and the other animal (day 14) showed spindle cell proliferation of smooth muscle cells (intermediate lesion). Focal periaortitis was seen in the same animal (day 7). C. pneumoniae elementary bodies were demonstrated by immunocytochemical stain in the lungs (n ‫؍‬ 2), liver (n ‫؍‬ 3), spleen (n ‫؍‬ 5), and aorta (n ‫؍‬ 2), one of which corresponded to the intermediate lesion. C. pneumoniae was cultured from the lungs (n ‫؍‬ 2), liver (n ‫؍‬ 2), spleen (n ‫؍‬ 2), and aortic arch (n ‫؍‬ 1). All histopathological, immunocytochemical, and cultural studies were negative in the controls. Hence, the rabbit provides a useful animal model for the study of C. pneumoniae infection and its complications, particularly atherosclerosis.

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“…Cell lines. RAW 264.7 cells (termed RAW cells), a murine macrophage cell line (ATCC CRL-24), and HEp-2 cells were maintained in Dulbecco medium supplemented with 10% fetal calf serum, glutamine, and antibiotics (19). U937 cells, a nonadherent human macrophage line, and McCoy cells were maintained in RPMI 1640 supplemented as described above.…”

Section: Methodsmentioning

confidence: 99%

“…After centrifugation for 1 h at 37ЊC at 800 ϫ g, the inoculum was removed and growth medium containing 1 g of cyclohexamide per ml was added. For McCoy cells and HEp-2 cells, growth medium was supplemented RPMI 1640 or Iscove's Dulbecco medium (19). For smooth muscle cells, smooth muscle growth medium (Clonetics) was used.…”

Section: Methodsmentioning

confidence: 99%

Replication of Chlamydia pneumoniae in vitro in human macrophages, endothelial cells, and aortic artery smooth muscle cells

et al. 1996

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Chlamydia pneumoniae has recently been associated with atherosclerotic lesions in coronary arteries. To investigate the biological basis for the dissemination and proliferation of this organism in such lesions, the in vitro growth of C. pneumoniae was studied in two macrophage cell lines, peripheral blood monocyte-derived macrophages, human bronchoalveolar lavage macrophages, several endothelial cell lines, and aortic smooth muscle cells. Five strains of C. pneumoniae were capable of three passages in human U937 macrophages and in murine RAW 246.7 macrophages. Titers were suppressed in both macrophage types with each passage, as compared with growth titers in HEp-2 cells. Both human bronchoalveolar lavage macrophages and peripheral blood monocyte-derived macrophages were able to inhibit C. pneumoniae after 96 h of growth. Eleven C. pneumoniae strains were capable of replicating in normal human aortic artery-derived endothelial cells, umbilical vein-derived endothelial cells, and pulmonary artery endothelial cells. Infection in human aortic artery smooth muscle cells was also established for 13 strains of C. pneumoniae. The in vitro ability of C. pneumoniae to maintain infections in macrophages, endothelial cells, and aortic smooth muscle cells may provide support for the hypothesis that C. pneumoniae can infect such cells and, when infection is followed by an immune response, may contribute to atheroma formation in vivo. More studies are needed to investigate the complex relationship between lytic infection and persistence and the potential for C. pneumoniae to influence the generation of atheromatous lesions. Chlamydia pneumoniae has been established as an important respiratory pathogen associated with 5 to 10% of communityacquired cases of pneumonia, pharyngitis, bronchitis, and sinusitis (3, 5, 7, 11-14, 25). In addition, C. pneumoniae infection has been associated with asthma, acute chest syndrome of sickle cell anemia, human immunodeficiency virus infection, Guillain-Barré syndrome, endocarditis, and otitis media and with patients with immunosuppressive diseases (1, 4, 8, 16, 17, 26-28). Cases of chronic persistent respiratory infection, in which antibiotic therapy failed to eradicate the organism, have also been reported (18). There is also evidence that C. pneumoniae can be cultured infrequently (2 and 4.5%, respectively) from asymptomatic and selectively healthy individuals (10, 20, 21). More recently, C. pneumoniae has been associated with coronary artery disease (24, 30, 31, 33, 34). The earliest serological association was reported by Saikku et al., who demonstrated an association of increased antibody titers to C. pneumoniae in men with acute myocardial infarction and chronic coronary heart disease (31). In another prospective study, they demonstrated that chronic C. pneumoniae infection may be a risk factor for the development of coronary heart disease (30). In the United States, Thom et al. reported a relationship between antibody to C. pneumoniae and angiographically demonstrated coronary artery di...

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Experimental infection with Chlamydia pneumoniae in nonhuman primates

Cited by 27 publications

References 11 publications

Identification of Chlamydia pneumoniae by DNA amplification of the 16S rRNA gene

Identification of Chlamydia pneumoniae by DNA amplification of the 16S rRNA gene

Rabbit model for Chlamydia pneumoniae infection

Replication of Chlamydia pneumoniae in vitro in human macrophages, endothelial cells, and aortic artery smooth muscle cells

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