Experimental infection of baboons (Papio cynocephalus anubis) with Chlamydia pneumoniae strain ‘TWAR’

Bell, Thomas A.; Kuo, Cho‐Chou; Wang, S.-P.; Grayston, J. T.

doi:10.1016/s0163-4453(89)94850-0

Cited by 14 publications

(4 citation statements)

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“…Previous animal studies have shown C. pneumoniae to cause mild but persistent infections (1, 7). Bell et al found low IgG titers and no IgM or tear antibodies over 8 weeks after baboon inoculation with a high titer of C. pneumoniae (1). Despite intratracheal instillation, no pulmonary infiltrates were seen on radiographs.…”

Section: Discussionmentioning

confidence: 98%

“…Reexposure to a larger inoculum resulted in mild conjunctivitis in only two of the three; the conjunctivitis was still more mild than in comparable C. trachomatisinoculated monkeys. Baboon ocular and respiratory inoculation with AR-39, another C. pneumoniae isolate, resulted in no apparent disease despite culture recovery intermittently over 8 weeks (1). Baboon inoculation with IOL-207, an organism similar if not identical to C. pneumoniae, into the eye, urethra, and knee joint caused clinical inflammation at those sites (3).…”

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confidence: 99%

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Experimental infection with Chlamydia pneumoniae in nonhuman primates

et al. 1990

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To serially examine the immunopathogenesis and histopathology of infection with Chlamydia pneumoniae, we inoculated two cynomolgus monkeys in the conjunctival sac, nose, and nasopharynx with C. pneumoniae TWAR. After inoculation, C. pneumoniae was isolated from the inoculation sites and the rectums of both monkeys for a period of 5 weeks. After a second inoculation, C. pneumoniae was recovered from the inoculation sites and the rectums of both monkeys for 20 weeks. A third inoculation with C. pneumoniae caused very little productive infection at any site. Prior C. pneumoniae infection did not prevent subsequent C. trachomatis serovar E (Bour strain) infection. Clinical and histopathologic ocular responses to C. pneumoniae infection were mild compared with those to infection with C. trachomatis serovar E. Rectal infection, demonstrated by culture isolation and immunohistopathology, occurred without direct experimental inoculation. Both immunofluorescent staining of mucosal smears with monoclonal antibodies and tissue culture were able to detect C. pneumoniae infection. Experimental nonhuman primate infection with C. pneumoniae appears to be clinically and histopathologically mild and can occur at extrapulmonary sites.

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Section: Discussionmentioning

confidence: 98%

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confidence: 99%

Experimental infection with Chlamydia pneumoniae in nonhuman primates

et al. 1990

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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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“…[5][6][7][8][9][10] Apolipoprotein (Apo) E-deficient knockout mice developed accelerated atherosclerosis if infected by intranasal inoculation. 11 Administration of macrolide antibiotics inhibited increased intimal thickening following intranasal inoculation in New Zealand White (NZW) rabbits fed with cholesterol-enriched diet.…”

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Chronic perivascular inoculation with Chlamydophila pneumoniae results in plaque formation in vivo

Engelmann

Redl

Pelisek

et al. 2006

Laboratory Investigation

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Hypercholesterolemic and normocholesterolemic rabbit models of chronic arterial Chlamydophila (Chlamydia) pneumoniae (CPN) inoculation were established and the role of both viable and inactivated bacteria was investigated in atherogenesis. A total of 29 rabbits were randomized to four groups. Groups A and B were fed a cholesterol-enriched diet, and groups C and D were fed a normal diet. Arterial segments of group A and C animals were inoculated in vivo using viable CPN chronically using repeated perivascular applications. Contralateral arteries were treated using heat-inactivated CPN. Group B and D animals were treated with repeated perivascular injections of bacterial lipopolysaccharide (LPS) and saline (control). Additional hypercholesterolemic rabbits were treated by repeated injections using viable and inactivated CPN, each controlled by saline injections. To compare the effects of this chronic inoculation model, additional animals received single injections of either viable CPN, inactivated CPN, LPS, or saline. Vascular tissues (n ¼ 162 treated arteries of 29 rabbits) were analyzed using morphometry at histology. CPN was detected by fluorescenceimmunohistochemistry and nested polymerase chain reaction. Only in hypercholesterolemic, but not in normocholesterolemic rabbits, chronic perivascular infection of all bacterial components, viable and heatinactivated CPN, as well as LPS resulted in a significant increase in atheromatous lesion formation (lesion area index: 0.2370.08, 0.2570.09, and 0.1570.05) when compared to controls (lesion area index 0.0170.01, P ¼ 0.002). CPN persisted in atheromatous lesions and vascular tissues. Single perivascular infection using CPN or inactivated CPN was not able to induce lesion formation (lesion area index: 0.0370.03, 0.0370.02 vs 0.0370.02 after single saline inoculation, P ¼ 0.965). In conclusion, chronic vascular infection with CPN or CPN components acts as a cofactor requiring other major atherogenic stimuli, rather than as a causative agent.

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Experimental infection of baboons (Papio cynocephalus anubis) with Chlamydia pneumoniae strain ‘TWAR’

Cited by 14 publications

References 5 publications

Experimental infection with Chlamydia pneumoniae in nonhuman primates

Experimental infection with Chlamydia pneumoniae in nonhuman primates

Rabbit model for Chlamydia pneumoniae infection

Chronic perivascular inoculation with Chlamydophila pneumoniae results in plaque formation in vivo

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