Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/30051
Conference/Presentation Title: Pro-inflammatory action of MIF in acute myocardial infarction through activation of peripheral blood mononuclear cells.
Authors: Morand E.F. ;Gao X.M.;Duffy S.J.;Dart A.M.;Du X.J.;White D.;Chan W.;Fang L.;Liu Y.;Taylor A.J.
Institution: (White, Fang, Liu, Du, Gao) Baker IDI Heart and Diabetes Institute, Melbourne, Australia (Chan, Taylor, Duffy, Dart) Heart Centre, Alfred Hospital, Melbourne, Australia (Morand) Monash Medical Centre, Melbourne, Australia
Presentation/Conference Date: 22-Sep-2011
Copyright year: 2011
Publisher: Oxford University Press
Publication information: European Heart Journal. Conference: European Society of Cardiology, ESC Congress 2011. Paris France. Conference Publication: (var.pagings). 32 (SUPPL. 1) (pp 579), 2011. Date of Publication: August 2011.
Abstract: Purpose: Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine, has been implicated in the pathogenesis of many inflammatory disorders. We investigated whether MIF acts as both a biomarker of cardiac injury and mediator of inflammatory responses following acute myocardial infarction (AMI). Method(s): 42 AMI patients, 10 stable angina patients and 10 healthy volunteers were recruited. Blood samples were collected at hospital admission (average 3 h after onset of AMI) and peripheral blood mononuclear cells (PBMCs) separated and cultured. Levels of MIF, matrix metalloproteinase-9 (MMP-9) and interleukin- 6 (IL-6) in both plasma and supernatant of cultured PBMC were measured by ELISA. Gene expression of these markers in PBMCs was determined by real-time PCR. PBMCs were cultured in control media or in the presence of COR100140 (an anti-MIF compound, 50 muM), neutralising anti-MIF antibody (10 ng/ml), IL-1beta (10 ng/ml), recombinant human MIF (rMIF, 5 ng/ml) or combination of IL-1beta and rMIF. AMI patients underwent cardiac magnetic resonance (CMR) examinations at day 3 and 3 months following AMI to measure left ventricular (LV) volumes, systolic function and infarct size. Result(s): Compared with controls, at day-1 post-AMI, plasma MIF levels were elevated by 2-3 fold and correlated positively with plasma levels of MMP-9 (r=0.64, P=0.01), IL-6 (r=0.70, P=0.004), peak troponin I (r=0.65, P<0.001) and creatine kinase (r=0.51, P<0.001). MIF plasma levels at day-1 post AMI also correlated positively with day-3 and 3 month CMR estimated infarct size (r=0.74, r=0.70, both P<0.001), LV end-diastolic (r=0.43, r=0.58, both P=0.005) and systolic volumes (r=0.63, r=0.60, both P<0.001), but negatively with LV ejection fraction (r=0.44, r=0.40, both P<0.02). Expression and production of MIF, MMP-9 and IL-6 by PBMCs were increased at day-3 (2-3 fold, P<0.05), but not at day-1 post-AMI. AMI or IL-1beta induced PBMC activation measured by up-regulation of MIF, MMP-9 and IL-6 (2-3 fold, P<0.05), which was attenuated by anti-MIF treatment. Further, IL-1beta-stimulated production of MMP-9 and IL-6 was significantly enhanced in the presence of exogenous rMIF by 35%. Conclusion(s): MIF is a key mediator of systemic and regional inflammation following AMI. Plasma MIF serves as a novel biomarker for myocardial inflammation and severity of tissue damage, and bears predictive values for acute and chronic dysfunction and remodelling post AMI. MIF inhibition attenuates PBMC activation induced by AMI or IL-1beta constituting a potential therapy to minimise inflammatory responses following AMI.
Conference Start Date: 2011-08-27
Conference End Date: 2011-08-31
DOI: http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1093/eurheartj/ehr323
ISSN: 0195-668X
URI: https://repository.monashhealth.org/monashhealthjspui/handle/1/30051
Type: Conference Abstract
Subjects: *society
human
plasma
inflammation
patient
infarction
blood level
heart ejection fraction
myocarditis
predictive value
therapy
upregulation
heart left ventricle volume
cardiovascular magnetic resonance
examination
pathogenesis
heart injury
stable angina pectoris
normal human
blood sampling
hospital admission
supernatant
gene expression
real time polymerase chain reaction
enzyme linked immunosorbent assay
interleukin 6
interleukin 1
gelatinase B
biological marker
antibody
troponin I
creatine kinase
factor A
macrophage migration inhibition factor
cytokine
marker
*peripheral blood mononuclear cell
tissue injury
*cardiology
*acute heart infarction
myocarditis
tissue injury
predictive value
therapy
upregulation
heart left ventricle volume
cardiovascular magnetic resonance
examination
pathogenesis
heart injury
stable angina pectoris
normal human
blood sampling
hospital admission
supernatant
gene expression
real time polymerase chain reaction
enzyme linked immunosorbent assay
infarction
patient
inflammation
plasma
human
*peripheral blood mononuclear cell
heart ejection fraction
*society
*acute heart infarction
*cardiology
blood level
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