Investigating the role of heat shock protein HSP60 in coronary artery disease patients infected with Helicobacter pylori

Muntadher Abdulateef Alhasan, Manal Badi Salih

Abstract


Background: Coronary artery disease is a disorder of the heart and blood vessels caused by the hardening or blockage of the coronary arteries. Elevated blood cholesterol, high blood sugar, and high blood pressure are prominent risk factors that contribute to the development of arterial hardening. Evaluation of heat shock protein 60 levels in patients with coronary artery disease infected with Helicobacter pylori bacteria and comparison of the results with non-infected patients and the control group.

Methods: This study was conducted in Nasiriyah Heart Center and Nasiriyah Teaching Hospital in Nasiriyah. A total of 150 samples were collected and divided into three groups: the first group consisted of patients with coronary artery disease infected with Helicobacter pylori bacteria, the second group consisted of patients with coronary artery disease but not infected with Helicobacter pylori, and the third group served as the control group. H. Pylori infection was determined in serum. Heat shock protein-60 levels were determined using enzyme-linked immunosorbent assay.

Results: The level of heat shock protein-60 in the first group was higher than that of the second and third groups, where (P = ≤0.001) and (LSD= 1.86).

Conclusion: Infection with certain pathogenic factors, such as bacteria, can lead to inflammation of the blood vessel lining, which in turn affects the development of coronary artery disease. Consequently, inflammatory factors can increase the cellular expression of heat shock proteins as a result of oxidative stress or inflammation. These heat shock proteins are then displayed on the cell surface and contribute to the presence of heat shock proteins in the blood. Efforts should be made to study heat shock proteins resulting from infection with pathogens, and their role in coronary artery disease and other heart diseases.


Full Text:

PDF

References


Adler SP, Hur JK, Wang J, Vetrovec GW. Prior infection with cytomegalovirus is not a major risk factor for angiographically demonstrated coronary artery atherosclerosis. Journal of Infectious Diseases, (1998); 177(1), 209–212.

Benjamin IJ, McMillan DR. Stress (heat shock) proteins molecular chaperones in cardiovascular biology and disease. Circulation Research, (1998); 83(2), 117–132.

Berk BC, Weintraub WS, Alexander RW. Elevation of C-reactive protein in “active” coronary artery disease. The American Journal of Cardiology, (1990); 65(3), 168–172.

Billack B, Heck DE, Mariano TM, Gardner, CR, Sur R, Laskin DL, Laskin JD. Induction of cyclooxygenase-2 by heat shock protein 60 in macrophages and endothelial cells. American Journal of Physiology - Cell Physiology, (2002); 283(4 52-4), 1267–1277.

Birnie DH, Holme ER, McKay IC, Hood S, McColl KEL, Hillis WS. Association between antibodies to heat shock protein 65 and coronary atherosclerosis. Possible mechanism of action of Helicobacter pylori and other bacterial infections in increasing cardiovascular risk. European Heart Journal, (1998); 19(3), 387–394.

Businaro R, Profumo E, Tagliani A, Buttari B, Leone S, D’Amati G, Ippoliti F, Leopizzi M, D’Arcangelo D, Capoano R, Fumagalli L, Salvati B, Riganò R. Heat-shock protein 90: A novel autoantigen in human carotid atherosclerosis. Atherosclerosis, (2009); 207(1), 74–83.

Chmiela M, Gajewski A, Rudnicka K. Helicobacter pylori vs coronary heart disease - searching for connections. World Journal of Cardiology, (2015); 7(4), 187.

de Graaf R, Kloppenburg G, Kitslaar PJHM, Bruggeman CA, Stassen F. Human heat shock protein 60 stimulates vascular smooth muscle cell proliferation through Toll-like receptors 2 and 4. Microbes and Infection, (2006); 8(7), 1859–1865.

De Nardin E. The role of inflammatory and immunological mediators in periodontitis and cardiovascular disease. Annals of Periodontology / the American Academy of Periodontology, (2001); 6(1), 30–40.

Epstein SE. The multiple mechanisms by which infection may contribute to atherosclerosis development and course. Circulation Research, (2002); 90(1), 2–4.

Epstein SE, Zhu J, Najafi AH, Burnett MS. Insights into the role of infection in atherogenesis and in plaque rupture. Circulation, (2009); 119(24), 3133–3141.

Haghighat N, Mohammadshahi M, Shayanpour S. The Relationship of Serum Heat Shock Protein 70 Antibody Levels with the Inflammatory Factors and Serum Uric Acid Levels in Hemodialysis Patients. Iranian Red Crescent Medical Journal, (2019); 21(6).

Hansson G K. Regulation of immune mechanisms in atherosclerosis. Annals of the New York Academy of Sciences, (2001); 947, 157–166.

Hoppichler F, Lechleitner M, Traweger C, Schett G, Dzien A, Sturm W, Qingbo X. Changes of serum antibodies to heat-shock protein 65 in coronary heart disease and acute myocardial infarction. Atherosclerosis, (1996); 126(2), 333–338.

Huang WS, Tseng CH, Lin CL, Tsai CH, Kao CH. Helicobacter pylori infection increases subsequent ischemic stroke risk: A nationwide population-based retrospective cohort study. Qjm, (2014); 107(12), 969–975.

Induce FT, Atherogenesis IOR. Inflammation or Atherogenesis. Health (San Francisco), (2008); 115–126.

Kocsis J, Veres A, Vatay A, Duba J, Karádi I, Füst G, Prohászka Z. Antibodies against the human heat shock protein hsp70 in patients with severe coronary artery disease. Immunological Investigations, (2002); 31(3–4), 219–231.

Lebherz-Eichinger D, Ankersmit HJ, Hacker S, Hetz H, Kimberger O, Schmidt EM, Reiter T, Hörl WH, Haas M, Krenn CG, Roth GA. HSP27 and HSP70 serum and urine levels in patients suffering from chronic kidney disease. Clinica Chimica Acta, (2012);413(1–2), 282–286.

Lopez LR, Dier KJ, Lopez D, Merrill JT, Fink CA. Anti-β2-Glycoprotein I and Antiphosphatidylserine Antibodies Are Predictors of Arterial Thrombosis in Patients with Antiphospholipid Syndrome. American Journal of Clinical Pathology, (2004); 121(1), 142–149.

Markus HS, Mendall MA. Helicobacter pylori infection: A risk factor for ischaemic cerebrovascular disease and carotid atheroma. Journal of Neurology Neurosurgery and Psychiatry, (1998); 64(1), 104–107.

Mohammed H, Alyasiri F. HbA1c as indicator for dyslipidaemia, cardiovascular and atherosclerotic events in patients with metabolic syndrome. University of Thi-Qar Journal of Science, (2019); 5(3).

Musiał K, Szprynger K, Szczepańska M, Zwolińska D. Heat shock proteins in children and young adults on chronic hemodialysis. Pediatric Nephrology, (2009); 24(10), 2029–2034.

Ohashi R, Mu H, Yao Q, Chen C. Atherosclerosis: Immunopathogenesis and immunotherapy. Medical Science Monitor, (2004); 10(11).

Ouchi K, Fujii B, Kanamoto Y, Karita M, Shirai M, Nakazawa T. Chlamydia pneumoniae in coronary and iliac arteries of Japanese patients with atherosclerotic cardiovascular diseases. Journal of Medical Microbiology, (1998); 47(10), 907–913.

Pencina MJ, Navar AM, Wojdyla D, Sanchez RJ, Khan I, Elassal J, D’agostino RB, Peterson ED, Sniderman AD. Quantifying Importance of Major Risk Factors for Coronary Heart Disease. Circulation, (2019); 139(13), 1603–1611.

Pockley AG. Heat shock proteins, inflammation, and cardiovascular disease. Circulation, (2002); 105(8), 1012–1017.

Prasad A, Zhu J, Halcox JPJ, Waclawiw MA, Epstein SE, Quyyumi AA. Predisposition to atherosclerosis by infections: Role of endothelial dysfunction. Circulation, (2002)106(2), 184–190.

Ridker PM. Evaluating novel cardiovascular risk factors: Can we better predict heart attacks? Annals of Internal Medicine, (1999); 130(11), 933–937.

Roger VL, Go AS, Lloyd-Jones, DM, Adams RJ, Berry JD, Brown TM, Carnethon MR., Dai S, De Simone G, Ford ES, Fox CS, Fullerton HJ, Gillespie C, Greenlund KJ, Hailpern SM, Heit JA, Michael Ho P, Howard VJ, Kissela BM, Wylie-Rosett J. Heart disease and stroke statistics-2011 update: A report from the American Heart Association. Circulation, (2011); 123(4).

Rosenfeld ME. Inflammation and atherosclerosis: Direct versus indirect mechanisms. Current Opinion in Pharmacology, (2013); 13(2), 154–160.

Schett G, Xu Q, Amberger A, Van Der Zee R, Recheis H, Willeit J, Wick G. Autoantibodies against heat shock protein 60 mediate endothelial cytotoxicity. Journal of Clinical Investigation, (1995); 96(6), 2569–2577.

Shoenfeld Y, Gerli R, Doria A, Matsuura E, Cerinic MM, Ronda N, Jara LJ, Abu-Shakra M, Meroni PL, Sherer Y. Accelerated atherosclerosis in autoimmune rheumatic diseases. Circulation, (2005); 112(21), 3337–3347.

Shoenfeld Y, Sherer Y, Harats D. Atherosclerosis as an infectious, inflammatory and autoimmune disease. Trends in Immunology, (2001); 22(6), 293–295.

Soehnlein O, Libby P. Targeting inflammation in atherosclerosis — from experimental insights to the clinic. Nature Reviews Drug Discovery, (2021); 20(8), 589–610.

Szodoray P, Timar O, Veres K, Der H, Szomjak E, Lakos G, Aleksza M, Nakken B, Szegedi G, Soltesz P. Th1/Th2 imbalance, measured by circulating and intracytoplasmic inflammatory cytokines - Immunological alterations in acute coronary syndrome and stable coronary artery disease. Scandinavian Journal of Immunology, (2006); 64(3), 336–344.

Vaughan CJ. Chronic infections and coronary heart disease. Lancet, (1997); 350(9083), 1029–1030.

Veres K, Lakos G, Kerényi A, Szekanecz Z, Szegedi G, Shoenfeld Y, Soltész P. Antiphospholipid antibodies in acute coronary syndrome. Lupus, (2004); 13(6), 423–427.

Visseren FLJ, MacH F, Smulders YM, Carballo D, Koskinas KC, Bäck M, Benetos A, Biffi A, Boavida JM, Capodanno D, Cosyns B, Crawford C, Davos CH, Desormais I, DI Angelantonio E, Franco O. H, Halvorsen S, Hobbs FDR, Hollander M, Williams B. 2021 ESC Guidelines on cardiovascular disease prevention in clinical practice. European Heart Journal, (2021); 42(34), 3227–3337.

Wick G, Jakic B, Buszko M, Wick MC, Grundtman C. The role of heat shock proteins in atherosclerosis. Nature Reviews Cardiology, (2014) 11(9), 516–529.

Xu Q, Wick G. The role of heat shock proteins in protection and pathophysiology of the arterial wall. Molecular Medicine Today, (1996); 2(9), 372–379.

Zhao Y, Zhang C, Wei X, Li P, Cui Y, Qin Y, Wei X, Jin M, Kohama K, Gao Y. Heat shock protein 60 stimulates the migration of vascular smooth muscle cells via Toll-like receptor 4 and ERK MAPK activation. Scientific Reports, (2015); 5(September), 1–11.




DOI: http://dx.doi.org/10.62940/als.v10i0.2058

Refbacks

  • There are currently no refbacks.