BACKGROUND: B-type natriuretic peptide (BNP) determination is routinely used to evaluate the severity of congestive heart failure, a possible consequence of coronary artery disease (CAD). CAD originates from vascular atherosclerotic processes and is stimulated by inflammatory events, which may also be triggered by chronic bacterial infections. AIM: To explore the effect of Helicobacter pylori infection upon systemic BNP, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and linear homology between cardiac peptides and H pylori. METHODS: A group of 103 consecutive patients with a diagnosis of non-ST elevation acute CAD (ACAD) and no other concomitant pathology was examined. BNP was measured by a commercial solid-phase sandwich immunoradiometric assay. H pylori infection, CagA serological status and circulating levels of IL-6 and TNF-α, were determined by ELISA assays. Amino acid sequence homology between human cardiac and H pylori peptides was investigated by Basic Local Alignment Search Tool (BLAST) analysis. RESULTS: Circulating levels of BNP and IL-6, in pg/mL (interquartile difference), among infected patients with anti-CagA serum antibodies, respectively 781 (1899) and 37.7 (137.6), were significantly increased in respect to those measured in uninfected patients, respectively 325 (655) and 7.7 (23.5), (p<0.01 and p=0.025), and, with regard to BNP alone, also in patients infected by CagA negative H pylori strains, 305 (593), (p<0.01). TNF-α levels were raised in CagA positive in respect to uninfected patients. Tropomyosin and Ca2+ transporting ATPases showed strong similarities to H pylori proteins, suggesting the existence of molecular mimicry phenomena. CONCLUSIONS: Chronic infection by H pylori expressing CagA correlates with high circulating levels of BNP and IL-6 in patients with ACAD.
Titolo: | Cross-sectional study: CagA-positive helicobacter pylori infection, acute coronary artery disease and systemic levels of B-type natriuretic peptide |
Autore/i: | Figura, N.; Palazzuoli, A.; VAIRA, BERARDINO; Campagna, M.; Moretti, E.; Iacoponi, F.; Giordano, N.; Clemente, S.; Nuti, R.; Ponzetto, A. |
Autore/i Unibo: | |
Anno: | 2014 |
Rivista: | |
Digital Object Identifier (DOI): | http://dx.doi.org/10.1136/jclinpath-2013-201743 |
Abstract: | BACKGROUND: B-type natriuretic peptide (BNP) determination is routinely used to evaluate the severity of congestive heart failure, a possible consequence of coronary artery disease (CAD). CAD originates from vascular atherosclerotic processes and is stimulated by inflammatory events, which may also be triggered by chronic bacterial infections. AIM: To explore the effect of Helicobacter pylori infection upon systemic BNP, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and linear homology between cardiac peptides and H pylori. METHODS: A group of 103 consecutive patients with a diagnosis of non-ST elevation acute CAD (ACAD) and no other concomitant pathology was examined. BNP was measured by a commercial solid-phase sandwich immunoradiometric assay. H pylori infection, CagA serological status and circulating levels of IL-6 and TNF-α, were determined by ELISA assays. Amino acid sequence homology between human cardiac and H pylori peptides was investigated by Basic Local Alignment Search Tool (BLAST) analysis. RESULTS: Circulating levels of BNP and IL-6, in pg/mL (interquartile difference), among infected patients with anti-CagA serum antibodies, respectively 781 (1899) and 37.7 (137.6), were significantly increased in respect to those measured in uninfected patients, respectively 325 (655) and 7.7 (23.5), (p<0.01 and p=0.025), and, with regard to BNP alone, also in patients infected by CagA negative H pylori strains, 305 (593), (p<0.01). TNF-α levels were raised in CagA positive in respect to uninfected patients. Tropomyosin and Ca2+ transporting ATPases showed strong similarities to H pylori proteins, suggesting the existence of molecular mimicry phenomena. CONCLUSIONS: Chronic infection by H pylori expressing CagA correlates with high circulating levels of BNP and IL-6 in patients with ACAD. |
Data stato definitivo: | 2015-12-24T10:25:33Z |
Appare nelle tipologie: | 1.01 Articolo in rivista |