Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs

Sorin V. Pislaru, Marc Van Ranst, Cristina D Pislaru, Zsolt Szelid, Gregor Theilmeier, J. M. Ossewaarde, Paul Holvoet, Stefan Janssens, Erik Verbeken, Frans J. Van De Werf

Research output: Contribution to journalArticle

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Abstract

Objectives: We evaluated the role of intracoronary, intrapulmonary and macrophage-mediated delivery of C. pneumoniae (Cp) on coronary lesion formation. Methods: Pigs were allocated to one of three coronary protocols (intracoronary, macrophage or control groups) or to a fourth - a pulmonary group. In the intracoronary group Cp was injected into the wall of the left anterior descending (LAD) and right coronary arteries (RCA) and vehicle into the circumflex (CX). In the macrophage group autologous macrophages preincubated with Cp or not were injected into the LAD and CX wall, respectively. Animals in the control group received vehicle in LAD and CX. In the pulmonary group aerosolised Cp was given intrabronchially, after a single injection of vehicle into the LAD wall. Delivery into the coronary artery wall was performed with a balloon catheter with low-profile injector ports. Results: Seroconversion occurred in the following proportions: 5/6 (intracoronary group), 4/5 (macrophage group), 0/6 (control group), and 1/6 (intrapulmonary group). Significantly higher maximal intimal thickness (MIT) was observed in LADs of intracoronary and pulmonary groups when compared to corresponding CXs. The presence of Cp antigen was associated with higher MIT (r=0.73; P<0.0001). Injection of macrophages into the coronary artery wall did not induce proliferation. Arteries without coronary interventions were morphologically normal. Conclusions: Intracoronary and intrapulmonary but not macrophage-mediated Cp inoculation were associated with moderate intimal proliferation in the absence of a lipid-rich diet. Pre-existing coronary lesions seem a prerequisite for Cp-induced proliferation.

Original languageEnglish (US)
Pages (from-to)834-842
Number of pages9
JournalCardiovascular Research
Volume57
Issue number3
DOIs
StatePublished - Mar 1 2003
Externally publishedYes

Fingerprint

Neointima
Chlamydophila pneumoniae
Coronary Vessels
Swine
Macrophages
Tunica Intima
Lung
Control Groups
Injections
Catheters
Diet
Lipids
Antigens

Keywords

  • Atherosclerosis
  • Coronary disease
  • Infection/inflammation
  • Macrophages

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Pislaru, S. V., Van Ranst, M., Pislaru, C. D., Szelid, Z., Theilmeier, G., Ossewaarde, J. M., ... Van De Werf, F. J. (2003). Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs. Cardiovascular Research, 57(3), 834-842. https://doi.org/10.1016/S0008-6363(02)00787-3

Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs. / Pislaru, Sorin V.; Van Ranst, Marc; Pislaru, Cristina D; Szelid, Zsolt; Theilmeier, Gregor; Ossewaarde, J. M.; Holvoet, Paul; Janssens, Stefan; Verbeken, Erik; Van De Werf, Frans J.

In: Cardiovascular Research, Vol. 57, No. 3, 01.03.2003, p. 834-842.

Research output: Contribution to journalArticle

Pislaru, SV, Van Ranst, M, Pislaru, CD, Szelid, Z, Theilmeier, G, Ossewaarde, JM, Holvoet, P, Janssens, S, Verbeken, E & Van De Werf, FJ 2003, 'Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs', Cardiovascular Research, vol. 57, no. 3, pp. 834-842. https://doi.org/10.1016/S0008-6363(02)00787-3
Pislaru, Sorin V. ; Van Ranst, Marc ; Pislaru, Cristina D ; Szelid, Zsolt ; Theilmeier, Gregor ; Ossewaarde, J. M. ; Holvoet, Paul ; Janssens, Stefan ; Verbeken, Erik ; Van De Werf, Frans J. / Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs. In: Cardiovascular Research. 2003 ; Vol. 57, No. 3. pp. 834-842.
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abstract = "Objectives: We evaluated the role of intracoronary, intrapulmonary and macrophage-mediated delivery of C. pneumoniae (Cp) on coronary lesion formation. Methods: Pigs were allocated to one of three coronary protocols (intracoronary, macrophage or control groups) or to a fourth - a pulmonary group. In the intracoronary group Cp was injected into the wall of the left anterior descending (LAD) and right coronary arteries (RCA) and vehicle into the circumflex (CX). In the macrophage group autologous macrophages preincubated with Cp or not were injected into the LAD and CX wall, respectively. Animals in the control group received vehicle in LAD and CX. In the pulmonary group aerosolised Cp was given intrabronchially, after a single injection of vehicle into the LAD wall. Delivery into the coronary artery wall was performed with a balloon catheter with low-profile injector ports. Results: Seroconversion occurred in the following proportions: 5/6 (intracoronary group), 4/5 (macrophage group), 0/6 (control group), and 1/6 (intrapulmonary group). Significantly higher maximal intimal thickness (MIT) was observed in LADs of intracoronary and pulmonary groups when compared to corresponding CXs. The presence of Cp antigen was associated with higher MIT (r=0.73; P<0.0001). Injection of macrophages into the coronary artery wall did not induce proliferation. Arteries without coronary interventions were morphologically normal. Conclusions: Intracoronary and intrapulmonary but not macrophage-mediated Cp inoculation were associated with moderate intimal proliferation in the absence of a lipid-rich diet. Pre-existing coronary lesions seem a prerequisite for Cp-induced proliferation.",
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T1 - Chlamydia pneumoniae induces neointima formation in coronary arteries of normal pigs

AU - Pislaru, Sorin V.

AU - Van Ranst, Marc

AU - Pislaru, Cristina D

AU - Szelid, Zsolt

AU - Theilmeier, Gregor

AU - Ossewaarde, J. M.

AU - Holvoet, Paul

AU - Janssens, Stefan

AU - Verbeken, Erik

AU - Van De Werf, Frans J.

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N2 - Objectives: We evaluated the role of intracoronary, intrapulmonary and macrophage-mediated delivery of C. pneumoniae (Cp) on coronary lesion formation. Methods: Pigs were allocated to one of three coronary protocols (intracoronary, macrophage or control groups) or to a fourth - a pulmonary group. In the intracoronary group Cp was injected into the wall of the left anterior descending (LAD) and right coronary arteries (RCA) and vehicle into the circumflex (CX). In the macrophage group autologous macrophages preincubated with Cp or not were injected into the LAD and CX wall, respectively. Animals in the control group received vehicle in LAD and CX. In the pulmonary group aerosolised Cp was given intrabronchially, after a single injection of vehicle into the LAD wall. Delivery into the coronary artery wall was performed with a balloon catheter with low-profile injector ports. Results: Seroconversion occurred in the following proportions: 5/6 (intracoronary group), 4/5 (macrophage group), 0/6 (control group), and 1/6 (intrapulmonary group). Significantly higher maximal intimal thickness (MIT) was observed in LADs of intracoronary and pulmonary groups when compared to corresponding CXs. The presence of Cp antigen was associated with higher MIT (r=0.73; P<0.0001). Injection of macrophages into the coronary artery wall did not induce proliferation. Arteries without coronary interventions were morphologically normal. Conclusions: Intracoronary and intrapulmonary but not macrophage-mediated Cp inoculation were associated with moderate intimal proliferation in the absence of a lipid-rich diet. Pre-existing coronary lesions seem a prerequisite for Cp-induced proliferation.

AB - Objectives: We evaluated the role of intracoronary, intrapulmonary and macrophage-mediated delivery of C. pneumoniae (Cp) on coronary lesion formation. Methods: Pigs were allocated to one of three coronary protocols (intracoronary, macrophage or control groups) or to a fourth - a pulmonary group. In the intracoronary group Cp was injected into the wall of the left anterior descending (LAD) and right coronary arteries (RCA) and vehicle into the circumflex (CX). In the macrophage group autologous macrophages preincubated with Cp or not were injected into the LAD and CX wall, respectively. Animals in the control group received vehicle in LAD and CX. In the pulmonary group aerosolised Cp was given intrabronchially, after a single injection of vehicle into the LAD wall. Delivery into the coronary artery wall was performed with a balloon catheter with low-profile injector ports. Results: Seroconversion occurred in the following proportions: 5/6 (intracoronary group), 4/5 (macrophage group), 0/6 (control group), and 1/6 (intrapulmonary group). Significantly higher maximal intimal thickness (MIT) was observed in LADs of intracoronary and pulmonary groups when compared to corresponding CXs. The presence of Cp antigen was associated with higher MIT (r=0.73; P<0.0001). Injection of macrophages into the coronary artery wall did not induce proliferation. Arteries without coronary interventions were morphologically normal. Conclusions: Intracoronary and intrapulmonary but not macrophage-mediated Cp inoculation were associated with moderate intimal proliferation in the absence of a lipid-rich diet. Pre-existing coronary lesions seem a prerequisite for Cp-induced proliferation.

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KW - Infection/inflammation

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