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      Putative consequences of exposure to Helicobacter pylori infection in patients with coronary heart disease in terms of humoral immune response and inflammation

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          Abstract

          Introduction

          Pathogens, including Helicobacter pylori (Hp), have been suggested to contribute to the development of coronary heart disease (CHD), although the evidence still remains insufficient. The study was focused on the exposure of CHD patients to Hp and resulting anti-Hp heat shock protein B HspB antibody production in relation to the level of serum lipopolysaccharide binding protein (LBP) as a marker of inflammation.

          Material and methods

          One hundred seventy CHD patients and 58 non-CHD individuals participated in this study. Coronary angiography confirmed the atheromatic background of CHD. The panel of classical risk factors included: arterial hypertension, diabetes, total cholesterol, low-density lipoprotein (LDL)/high-density lipoprotein (HDL) cholesterol, triglycerides, obesity and nicotinism. The Hp status was estimated by 13C urea breath test and serology. Immunoblot and ELISA were used for screening the sera samples for anti-Hp HspB immunoglobulins (Igs) and LBP.

          Results

          Coronary heart disease patients were exposed to Hp more frequently than non-CHD individuals. This was associated with increased levels of specific anti-Hp IgG2 and IgA as well as total IgA. Hp infected CHD and non-CHD donors produced anti-Hp HspB IgG cross-reacting with human Hsp 60. In CHD patients the LBP level was significantly higher in comparison to non-CHD donors. This was related to the severity of the disease. Type I Hp strains stimulated higher LBP levels than less pathogenic type II isolates.

          Conclusions

          Lipopolysaccharide binding protein secreted in excess together with anti-Hp HspB, cross-reacting with human Hsp60, may increase the risk of vascular pathologies in Hp-exposed CHD patients.

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          Pathophysiology of coronary artery disease.

          Peter Libby, Pierre Théroux (2005)
          During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.
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            Fibrinogen stimulates macrophage chemokine secretion through toll-like receptor 4.

            George King, S D Smiley, Robert E. W. Hancock (2001)
            Extravascular fibrin deposition is an early and persistent hallmark of inflammatory responses. Fibrin is generated from plasma-derived fibrinogen, which escapes the vasculature in response to endothelial cell retraction at sites of inflammation. Our ongoing efforts to define the physiologic functions of extravasated fibrin(ogen) have led to the discovery, reported here, that fibrinogen stimulates macrophage chemokine secretion. Differential mRNA expression analysis and RNase protection assays revealed that macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, MIP-2, and monocyte chemoattractant protein-1 are fibrinogen inducible in the RAW264.7 mouse macrophage-like cell line, and ELISA confirmed that both RAW264.7 cells and primary murine thioglycolate-elicited peritoneal macrophages up-regulate the secretion of monocyte chemoattractant protein-1 >100-fold upon exposure to fibrinogen. Human U937 and THP-1 precursor-1 (THP-1) monocytic cell lines also secreted chemokines in response to fibrinogen, upon activation with IFN-gamma and differentiation with vitamin D(3), respectively. LPS contamination could not account for our observations, as fibrinogen-induced chemokine secretion was sensitive to heat denaturation and was unaffected by the pharmacologic LPS antagonist polymyxin B. Nevertheless, fibrinogen- and LPS-induced chemokine secretion both apparently required expression of functional Toll-like receptor 4, as each was diminished in macrophages derived from C3H/HeJ mice. Thus, innate responses to fibrinogen and bacterial endotoxin may converge at the evolutionarily conserved Toll-like recognition molecules. Our data suggest that extravascular fibrin(ogen) induces macrophage chemokine expression, thereby promoting immune surveillance at sites of inflammation.
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              Relation of Helicobacter pylori infection and coronary heart disease.

              Ahmed T Toosy, D. W. Strachan, Benjamin J Levy … (1994)
              There is evidence suggesting that early life experience may influence adult risk of coronary heart disease (CHD). Chronic bacterial infections have been associated with CHD. To determine whether Helicobacter pylori, a childhood acquired chronic bacterial infection, is associated with an increased risk of coronary heart disease in later life. Case-control study controlling for potential confounding variables with an opportunistically recruited control group. 111 consecutive cases with documented CHD were recruited from a cardiology clinic and 74 controls from a general practice health screening clinic. All were white men aged 45-65. Serum was analysed for the presence of H pylori specific IgG antibodies by ELISA (98% sensitive and 94% specific for the presence of infection). 59% of the cases and 39% of the controls were seropositive for H pylori (odds ratio 2.28, chi 2 7.35, p = 0.007). After adjustment by multiple logistic regression for age, cardiovascular risk factors, and current social class, the effect of H pylori was little altered (odds ratio 2.15, p = 0.03). Further adjustment for various features of the childhood environment known to be risk factors for H pylori infection only slightly weakened the association (odds ratio 1.9). H pylori seropositivity was not related to the level of risk factors in the control population. In this pilot study the association of adult coronary heart disease with H pylori seropositivity suggests that the early childhood environment may be important in determining the risk of CHD in adult life. The association needs confirmation in other better designed studies. If H pylori itself is responsible for the association, then this is of great potential importance as the infection is treatable.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arch Med Sci
                Journal ID (iso-abbrev): Arch Med Sci
                Journal ID (publisher-id): AMS
                Title: Archives of Medical Science : AMS
                Publisher: Termedia Publishing House
                ISSN (Print): 1734-1922
                ISSN (Electronic): 1896-9151
                Publication date (Electronic): 02 February 2016
                Publication date (Print): 01 February 2016
                Volume: 12
                Issue: 1
                Pages: 45-54
                Affiliations
                [1 ]Laboratory of Gastroimmunology, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland
                [2 ]Department of Internal Diseases and Clinical Pharmacology, Biegański Regional Specialty Hospital, Medical University of Lodz, Lodz, Poland
                [3 ]II Cardiology Clinic, Bieganski Regional Specialty Hospital, Medical University of Lodz, Lodz, Poland
                [4 ]Biobank Lab, Department of Molecular Biophysics, Institute of Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland
                Author notes
                Corresponding author: Karolina Rudnicka, Laboratory of Gastroimmunology, Department of Immunology and Infectious Biology, Faculty of Biology and Environmental Protection University of Lodz, 12/16 Banacha St, 90-237 Lodz, Poland. Phone: +48 42 635 45 25. E-mail: rudnicka@ 123456biol.uni.lodz.pl
                Article
                Publisher ID: 24977
                DOI: 10.5114/aoms.2015.50772
                PMC ID: 4754360
                PubMed ID: 26925118
                SO-VID: a4eb70ff-203d-40f7-8116-919357b6ef13
                Copyright © Copyright © 2016 Termedia & Banach
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                Date received : 27 February 2014
                Date accepted : 03 June 2014
                Categories
                Subject: Clinical Research

                ScienceOpen disciplines: Medicine
                Keywords: atherosclerosis,helicobacter pylori,autoantibodies,heat shock protein,lipopolysaccharide binding protein
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: atherosclerosis, helicobacter pylori, autoantibodies, heat shock protein, lipopolysaccharide binding protein

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