Lifestyle intervention is associated with decreased concentrations of circulating pentraxin 3 independent of CRP decrease

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Abstract

Objectives

Pentraxin 3 (PTX3) is an acute phase marker, which is produced at the site of infection or inflammation in contrast to CRP that is mainly synthesized by the liver. The aim of the present study was to see if lifestyle interventions/weight loss would lead to decreased blood plasma concentrations of PTX3.

Methods

Study subjects ( n = 31) were recruited to a lifestyle intervention program aiming at increased physical activity, improved eating habits, and weight loss. High-sensitivity C-reactive protein (CRP) and PTX3 methods were used for analysis of CRP and PTX3 in plasma samples collected at inclusion and after 4 and 8 weeks of treatment.

Results

Wilcoxon paired samples test showed a significant decrease in PTX3 concentrations from 2068 pg/mL at start to 2007 pg/mL at 4 weeks ( P = 0.002) and 1748 pg/mL at 8 weeks ( P = 0.003). The PTX3 decrease was not significantly correlated with a corresponding decrease in CRP or weight reduction.

Conclusions

The lifestyle intervention program resulted in a significant reduction of circulating concentrations of pentraxin 3 already after 4 and 8 weeks of treatment.

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Most cited references 18

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PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans.

T Moccetti, M Metra, R Latini … (2000)

Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested. Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94+/-11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P 64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes. PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy.

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Cardioprotective function of the long pentraxin PTX3 in acute myocardial infarction.

Monica Salio, Stefano Chimenti, Noeleen De Angelis … (2008)

Despite widespread clinical use as a prognostic marker in ischemic heart disorders, the actual pathogenetic role of the short pentraxin, C-reactive protein, has not undergone stringent genetic testing because of evolutionary divergence between mouse and humans. The long pentraxin PTX3 is conserved in evolution, is expressed in the heart under inflammatory conditions, and is a candidate prognostic marker in acute myocardial infarction. It was therefore important to assess whether PTX3 plays a pathogenetic role in acute myocardial infarction. In a model of acute myocardial infarction caused by coronary artery ligation and reperfusion, tissue mRNA expression and circulating levels of PTX3 increased. The interleukin-1R-MyD88 pathway plays a pivotal role in the induction of PTX3 transcript after ischemia. ptx3-deficient mice showed exacerbated heart damage (33% larger infarcts in null mice; P=0.0047). Increased myocardial damage in ptx3-deficient mice was associated with a greater no-reflow area, increased neutrophil infiltration, decreased number of capillaries, and increased number of apoptotic cardiomyocytes. In addition, ptx3-deficient mice with acute myocardial infarction showed higher circulating levels of interleukin-6 and increased C3 deposition in lesional tissue. The phenotype was reversed by exogenous PTX3. Thus, PTX3 plays a nonredundant, regulatory, cardioprotective role in acute myocardial infarction in mice. Our results suggest that modulation of the complement cascade contributes to the cardioprotective function of PTX3.

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Deficiency of the long pentraxin PTX3 promotes vascular inflammation and atherosclerosis.

A. V. Venu Gopal, Cecilia Garlanda, P. MARCHESI … (2009)

Immune responses participate in several phases of atherosclerosis; there is, in fact, increasing evidence that both adaptive immunity and innate immunity tightly regulate atherogenesis. Pentraxins are a superfamily of acute-phase proteins that includes short pentraxins such as C-reactive protein or long pentraxins such as PTX3, a molecule acting as the humoral arm of innate immunity. To address the potential role of PTX3 in atherogenesis, we first investigated the expression of PTX3 during atherogenesis, generated double-knockout mice lacking PTX3 and apolipoprotein E, and then studied the effect of murine PTX3 deficiency on plasma lipids, atherosclerosis development, and gene expression pattern in the vascular wall. PTX3 expression increases in the vascular wall of apolipoprotein E-knockout mice from 3 up to 18 months of age. Double-knockout mice lacking PTX3 and apolipoprotein E were fed an atherogenic diet for 16 weeks. Aortic lesions were significantly increased in double-knockout mice and mice heterozygous for PTX3 compared with apolipoprotein E-knockout mice. Mice lacking PTX3 showed a more pronounced inflammatory profile in the vascular wall as detected by cDNA microarray and quantitative polymerase chain reaction analysis and an increased macrophage accumulation within the plaque. Finally, lesion size correlated with the number of bone marrow monocytes. PTX3 has atheroprotective effects in mice, which, in light of the cardioprotective effects recently reported, suggests a cardiovascular protective function of the long pentraxin 3 through the modulation of the immunoinflammatory balance in the cardiovascular system.

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Author and article information

Journal

Journal ID (nlm-ta): Ups J Med Sci

Journal ID (iso-abbrev): Ups. J. Med. Sci

Journal ID (publisher-id): UPS

Title: Upsala Journal of Medical Sciences

Publisher: Informa Healthcare

ISSN (Print): 0300-9734

ISSN (Electronic): 2000-1967

Publication date (Print): August 2013

Publication date (Electronic): 03 July 2013

Volume: 118

Issue: 3

Pages: 165-168

Affiliations

Department of Medical Sciences, Clinical Chemistry, Uppsala University , Uppsala, Sweden

Author notes

Correspondence: Torbjörn Åkerfeldt, Department of Medical Sciences, Section of Clinical Chemistry, Akademiska Sjukhuset , entrance 61, 2nd floor, SE-751 85 Uppsala, Sweden. +46 18 611 37 03. torbjorn.akerfeldt@ 123456akademiska.se

Article

Publisher ID: UPS_A_801540_O

DOI: 10.3109/03009734.2013.801540

PMC ID: 3713381

PubMed ID: 23837595

SO-VID: 1e4a16e1-2105-409b-87b9-904b8e2e4889

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

History

Date received : 23 January 2013

Date accepted : 29 April 2013

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