In vitro infection and pathogenesis of Chlamydia pneumoniae in endovascular cells☆,☆☆
Section snippets
Growth in vascular cells
C pneumoniae can grow in vascular cells of various types and can be passaged in them.21 To investigate the biological basis for the dissemination and proliferation of this organism in atherosclerotic lesions, the in vitro growth of C pneumoniae was studied in 2 macrophage cell lines, peripheral blood monocyte (PBMC)-derived macrophages, human bronchoalveolar lavage (BAL) macrophages, several endothelial cell lines (human umbilical vein cells, pulmonary artery endothelial cells, and aortic
Growth in coronary artery endothelial cells and transmission of infection
To determine whether C pneumoniae was (1) capable of growing in endothelial cells derived from human cadaver coronary artery endothelial cells (CAEC) and (2) whether macrophages that were infected with C pneumoniae were capable of transmitting the infection to endothelial cells when they were brought into contact with the endothelial cells in culture, a study was performed with the use of a coronary isolate of C pneumoniae A-03.22 U-937 human macrophages infected with C pneumoniae were brought
Cytokine response of macrophages infected with C pneumoniae
We have investigated whether C pneumoniae can induce various cytokine responses when macrophages were infected with the organism23 because it has been postulated that alveolar macrophages may play a role in the initial pulmonary infectious process. To study the cytokine response of U-937 cells, a nonadherent human monocyte/macrophage cell line, infected in vitro with C pneumoniae , strain 2023, 4 mL of 106 cells/mL were infected with 1 mL of 3.5 × 104 IFU/mL of C pneumoniae by gentle agitation
IL-8 response of human coronary artery endothelial cells infected with C pneumoniae
Preliminary data have demonstrated the ability of C pneumoniae strain A-03 to elicit an IL-8 response in coronary artery endothelial cells.24 IL-8 was produced by cells that were inoculated with both viable and nonviable C pneumoniae , but levels were higher for viable organisms at time points of 24, 48, and 72 hours. At 48 hours, levels peaked at 1221.6 pg/mL for cells infected with viable C pneumoniae compared with 1023.6 pg/mL for cells inoculated with killed organisms and 944.4 pg/mL for
Interferon-γ restricted growth of C pneumoniae in cells
Additionally, we have investigated the role of interferon in restricting the growth of C pneumoniae in HEp-2 cells and U-937 macrophages.25 Persistent infection in macrophages could mediate the transport of C pneumoniae to vascular lesions. Cytokines, such as IFN-γ, have been demonstrated to restrict the growth of intracellular pathogens, such as C trachomatis . The role of IFN-γ on intracellular growth of C pneumoniae was investigated in human U-937 macrophages and HEp-2 cells (Table III).
References (27)
- et al.
Is atherosclerosis an immunologically mediated disease?
Immunology Today
(1995) - et al.
Chronic infections and coronary heart disease: is there a link?
Lancet
(1997) Inflammation and coronary artery disease
N Engl J Med
(1994)- et al.
Site of intimal rupture or erosion of thrombosed coronary athero-sclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology
Circulation
(1994) - et al.
Isolation of Chlamydia pneumoniae from a carotid endarterectomy specimen
J Infect Dis
(1997) - et al.
Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study
Ann Intern Med
(1992) - et al.
Serological evidence of an association of a novel chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction
Lancet
(1988) Chlamydia pneumoniae infection as a risk factor in acute myocardial infarction
Eur Heart J
(1993)- et al.
Detection of Chlamydia pneumoniae in coronary arterial fatty streaks and atheromatous plaques
South African Med J
(1992) - et al.
Detection of Chlamydia pneumoniae TWAR in human coronary atherectomy tissues
J Infect Dis
(1995)
High prevalence of Chlamydia pneumoniae DNA in peripheral blood mononuclear cells in patients with cardiovascular disease and in middle-aged blood donors
J Infect Dis
Animal models for Chlamydia pneumoniae infection
Scand J Infect Dis
Rabbit model for Chlamydia pneumoniae refection
J Clin Microbiol
Cited by (55)
Jurkat cell proliferation is suppressed by Chlamydia (Chlamydophila) pneumoniae infection accompanied with attenuation of phosphorylation at Thr389 of host cellular p70S6K
2013, ImmunobiologyCitation Excerpt :Many studies have reported the preferred host cell types for C. pneumoniae. C. pneumoniae can infect and multiply in endothelial cells, aortic smooth muscle cells, monocytes/macrophages (Gaydos et al. 1996; Godzik et al. 1995; Kalayoglu et al. 2001; Quinn and Gaydos 1999; Airenne et al. 1999), and lymphocytes (Haranaga et al. 2001a,b; Yamaguchi et al. 2002a,b). It has been hypothesized that circulating monocytes or lymphocytes infected with C. pneumoniae may act as carriers of the bacteria from the respiratory tract to the peripheral endothelial or smooth muscle cells, or as a reservoir of infected C. pneumoniae near and at the lesion in the development and progression of atherosclerosis.
Chlamydia-induced reactive arthritis: Hidden in plain sight?
2011, Best Practice and Research: Clinical RheumatologyCitation Excerpt :In vitro data suggest that background cytokine and chemokine levels in the host are important in promoting or maintaining persistent chlamydial infections. It has been well documented in several different laboratories that decreased expression of tumour necrosis factor (TNF)-alpha and/or interferon (IFN)-gamma promotes the persistent state, and as levels of these two cytokines decrease, chlamydial replication increases [71–75]. A Chlamydia-induced animal model demonstrated that susceptible rats mounted a lesser initial TNF-alpha, IFN-gamma and interleukin-4 (IL-4) response to an acute infection with C. trachomatis compared with non-susceptible rats [76].
Reactive Arthritis: Defined Etiologies, Emerging Pathophysiology, and Unresolved Treatment
2006, Infectious Disease Clinics of North AmericaCitation Excerpt :Lower levels of TNF-α have been demonstrated in ReA compared with other types of inflammatory arthritis, and ReA is believed to be more of a Th2-driven disease [90–92]. Also, in vitro data suggest that persistent Ct and Cpn levels are inversely associated with TNF-α levels [95–99]. There are no randomized trials in ReA to assess accurately their efficacy in this setting.
Statins and Reduction of Stroke: Cholesterol-Lowering versus Pleiotropic Effects
2004, Statins: Understanding Clinical Use
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