ORIGINAL ARTICLE
HSP60, SP110 and TNF-α expression in Chlamydia pneumoniae-positive versus Chlamydia pneumoniae-negative atherosclerotic plaques
1
Clinical Centre of Montenegro, Montenegro
2
Faculty of Medicine, University of Montenegro, Montenegro
Submission date: 2021-04-28
Final revision date: 2022-01-29
Acceptance date: 2022-03-05
Publication date: 2022-03-08
Pol J Pathol 2021;72(4):338-345
KEYWORDS
TOPICS
ABSTRACT
Traditionally recognized risk factors for atherosclerosis are not presented in 50% of patients with ischemic heart disease. Chronic inflammation with low pathogenic agents with slightly, or no signs of inflammation is the mainstay of atherosclerosis and could be triggered by an infectious agent, most commonly by Chlamydia pneumoniae.
Immunostaning of 33 Chlamydia pneumoniae-positive and 30 Chlamydia pneumoniae-
negative quadriple arterial sets were examined for protective Sp110, and atherogenic HSP60 markers, as well as for TNF-α which is inflammatory marker affected by both of them.
The Chlamydia pneumoniae-negative deceased subjects were statistically significantly older and their BMI was significantly lower. The results showed that age, hypercholesterolemia, diabetes, arterial hypertension and BMI were negatively correlated with Chlamydia pneumoniae-positivity, while no significant relationship was found between Chlamydia pneumoniae-positivity and a positive family history of cardiovascular diseases, as well as smoking. Significantly higher presence of Sp110 in Chlamydia pneumoniae-negative group versus significantly higer presence od HSP60 in Chlamydia pneumoniae-positive group. Chlamydia pneumoniae-negative plaques showed higher TNF-α expression; difference is present for all arteries examined except the Willis circle.
This study may provide a model for further understanding the mechanisms of Chlamydia pneumoniae atherogenesis and evaluating chlamydial intervention strategies for preventing the advancement of atherosclerotic lesions enhanced by bacterial infections.
Immunostaning of 33 Chlamydia pneumoniae-positive and 30 Chlamydia pneumoniae-
negative quadriple arterial sets were examined for protective Sp110, and atherogenic HSP60 markers, as well as for TNF-α which is inflammatory marker affected by both of them.
The Chlamydia pneumoniae-negative deceased subjects were statistically significantly older and their BMI was significantly lower. The results showed that age, hypercholesterolemia, diabetes, arterial hypertension and BMI were negatively correlated with Chlamydia pneumoniae-positivity, while no significant relationship was found between Chlamydia pneumoniae-positivity and a positive family history of cardiovascular diseases, as well as smoking. Significantly higher presence of Sp110 in Chlamydia pneumoniae-negative group versus significantly higer presence od HSP60 in Chlamydia pneumoniae-positive group. Chlamydia pneumoniae-negative plaques showed higher TNF-α expression; difference is present for all arteries examined except the Willis circle.
This study may provide a model for further understanding the mechanisms of Chlamydia pneumoniae atherogenesis and evaluating chlamydial intervention strategies for preventing the advancement of atherosclerotic lesions enhanced by bacterial infections.
REFERENCES (42)
1.
Libby P. Coronary artery injury and the biology of atherosclerosis: inflammation, thrombosis, and stabilization. Am J Cardiol 2000; 86 (8B): 3J-8J.
2.
Renko J Bacterial DNA signatures in arterial inflammation [academic dissertation], University of Tampere, 2008.
3.
Dabiri H, Rezadehbashi M, Badami N, et al. Detection of Chlamydia pneumoniae in atherosclerotic plaques of patients in Tehran, Iran. Jpn J Infect Dis 2009; 62: 195-197.
4.
Epstein SE. The multiple mechanisms by which infection may contribute to atherosclerosis development and course. Circ Res 2002; 90: 2-4.
5.
Honarmand H. Atherosclerosis Induced by Chlamydophila pneumoniae: A Controversial Theory. Interdiscip Perspect Infect Dis 2013; 2013: 941392.
6.
Di Pietro M, Filardo S, De Santis F, Sessa R. Chlamydia pneumoniae infection in atherosclerotic lesion development through oxidative stress: a brief overview. Int J Mol Sci 2013; 14: 15105-15120.
7.
Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation 1999; 100: e20-8.
8.
Pothineni NVK, Subramany S, Kuriakose K, et al. Infections, atherosclerosis, and coronary heart disease. Eur Heart J 2017; 38: 3195-3201.
9.
Lalla E, Lamster IB, Hofmann MA, et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003; 23: 1405-1411.
10.
Shah PK. Inflammation, infection and atherosclerosis. Trends Cardiovasc Med 2019; 29: 468-472.
11.
Bachmaier K, Neu N, de la Maza LM, Pal S, et al. Chlamydia infections and heart disease linked through antigenic mimicry. Science 1999; 283: 1335-1339.
12.
Leu JS, Chen ML, Chang SY, et al. SP110b Controls Host Immunity and Susceptibility to Tuberculosis. Am J Respir Crit Care Med 2017; 195: 369-382.
13.
Kramnik I, Dietrich WF, Demant P, Bloom BR. Genetic control of resistance to experimental infection with virulent Mycobacterium tuberculosis. Proc Natl Acad Sci U S A 2000; 97: 8560-8565.
14.
Pan H, Yan BS, Rojas M, et al. Ipr1 gene mediates innate immunity to tuberculosis. Nature 2005; 434: 767-772.
15.
Bloch DB, Nakajima A, Gulick T, et al. Sp110 localizes to the PML-Sp100 nuclear body and may function as a nuclear hormone receptor transcriptional coactivator. Mol Cell Biol 2000; 20: 6138-6146.
16.
Izadi M, Fazel M, Akrami M, et al. Chlamydia pneumoniae in the atherosclerotic plaques of coronary artery disease patients. Acta Med Iran 2013; 51: 864-870.
17.
Sessa R, Di Pietro M, Schiavoni G, et al. Chlamydia pneumoniae DNA in patients with symptomatic carotid atherosclerotic disease. J Vasc Surg 2003; 37: 1027-1031.
18.
Frutos MC, Monetti MS, Mosmann J, et al. Molecular characterization of Chlamydia pneumoniae in animals and humans from Argentina: Genetic characterization of Chlamydia pneumoniae. Infect Genet Evol 2016; 44: 43-45.
19.
Sessa R, Di Pietro M, Schiavoni G, et al. Chlamydia pneumoniae in asymptomatic carotid atherosclerosis. Int J Immunopathol Pharmacol 2006; 19: 111-118.
20.
Player MS, Mainous AG 3rd, Everett CJ, Diaz VA, et al. Chlamydia pneumoniae and progression of subclinical atherosclerosis. Eur J Prev Cardiol 2014; 21: 559-565.
21.
Wong YK, Gallagher PJ, Ward ME. Chlamydia pneumoniae and atherosclerosis. Heart 1999; 81: 232-238.
22.
Assar O, Nejatizadeh A, Dehghan F, et al. Association of Chlamydia pneumoniae Infection With Atherosclerotic Plaque Formation. Glob J Health Sci 2015; 8 (4): 260-267.
23.
Yazouli LE, Hejaji H, Elmdaghri N, et al. Investigation of Chlamydia pneumoniae infection in Moroccan patients suffering from cardiovascular diseases. J Infect Public Health 2018; 11: 246-249.
24.
Xu Q. Role of heat shock proteins in atherosclerosis. Arterioscler Thromb Vasc Biol 2002; 22: 1547-1559.
25.
Deniset JF, Hedley TE, Hlaváčková M, et al. Heat shock protein 60 involvement in vascular smooth muscle cell proliferation. Cell Signal 2018; 47: 44-51.
26.
Kern JM, Maass V, Maass M. Chlamydia pneumoniae-induced pathological signaling in the vasculature. FEMS Immunol Med Microbiol 2009; 55: 131-139.
27.
Rupp J, Hellwig-Burgel T, Wobbe V, et al Chlamydia pneumoniae infection promotes a proliferative phenotype in the vasculature through Egr-1 activation in vitro and in vivo. Proc Natl Acad Sci U S A 2005; 102: 3447-3452.
28.
Kol A, Bourcier T, Lichtman AH, Libby P. Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages. J Clin Invest 1999; 103: 571-577.
29.
Mosorin M, Surcel HM, Laurila A, et al. Detection of Chlamydia pneumoniae-reactive T lymphocytes in human atherosclerotic plaques of carotid artery. Arterioscler Thromb Vasc Biol 2000; 20: 1061-1067.
30.
Wick C. Tolerization against atherosclerosis using heat shock protein 60. Cell Stress Chaperones 2016; 21: 201-211.
31.
Knoflach M, Kiechl S, Mayrl B, et al. T-cell reactivity against HSP60 relates to early but not advanced atherosclerosis. Atherosclerosis 2007; 195: 333-338.
32.
Mussa FF, Chai H, Wang X, et al. Chlamydia pneumoniae and vascular disease: an update. J Vasc Surg 2006; 43: 1301-1307.
33.
Hu Y, Chen Z, Jiang L, Chen F, Jin R, Cheng L. Effects of oral and subcutaneous administration of HSP60 on myeloid-derived suppressor cells and atherosclerosis in ApoE-/- mice. Biochem Biophys Res Commun 2018; 498 (4): 701-706.
34.
Bahamondez-Canas TF, Cui Z. Intranasal immunization with dry powder vaccines. Eur J Pharm Biopharm 2018; 122: 167-175.
35.
Kuroda S, Kobayashi T, Ishii N, et al. Role of Chlamydia pneumoniae-infected macrophages in atherosclerosis developments of the carotid artery. Neuropathology 2003; 23: 1-8.
36.
Knoflach M, Bernhard D, Wick G. Anti-HSP60 immunity is already associated with atherosclerosis early in life. Ann N Y Acad Sci 2005; 1051: 323-331.
37.
Wick G, Knoflach M, Xu Q. Autoimmune and inflammatory mechanisms in atherosclerosis. Annu Rev Immunol 2004; 22: 361-403.
38.
Bodolay E, Prohászka Z, Paragh G, et al. Increased levels of anti-heat-shock protein 60 (anti-Hsp60) indicate endothelial dysfunction, atherosclerosis and cardiovascular diseases in patients with mixed connective tissue disease. Immunol Res 2014; 60: 50-59.
39.
Zafiratos MT, Cottrell JT, Manam S, et al. Tumor necrosis factor receptor superfamily members 1a and 1b contribute to exacerbation of atherosclerosis by Chlamydia pneumoniae in mice. Microbes Infect 2019; 21: 104-108.
40.
Janczak D, Ziolkowski P, Szyde³ko T, et al. The presence of some cytokines and Chlamydia pneumoniae in the atherosclerotic carotid plaque in patients with carotid artery stenosis. Postepy Hig Med Dosw (Online) 2015; 69: 227-232.
41.
Filardo S, Di Pietro M, Farcomeni A, et al. Chlamydia pneumoniae-Mediated Inflammation in Atherosclerosis: A Meta-Analysis. Mediators Inflamm 2015; 2015: 378658.
42.
Oksaharju A, Lappalainen J, Tuomainen AM, et al. Pro-atherogenic lung and oral pathogens induce an inflammatory response in human and mouse mast cells. J Cell Mol Med 2009; 13: 103-113.
| eISSN: | 2084-9869 |
| ISSN: | 1233-9687 |
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