Elevated Plasma C-Reactive Protein in Chronically Distressed Subjects Who Carry the A Allele of the TNF-α −308 G/A Polymorphism

Jeanmonod, Pascal; Känel, Roland von; Maly, Friedrich E.; Fischer, Joachim E.

doi:10.1097/01.psy.0000130903.78444.7d

Cited by 51 publications

(20 citation statements)

References 33 publications

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“…The G allele frequency in TNFB 252A [ G polymorphism was 24%, which is in accordance with another report from a North Indian population (21.29%) [24]. Higher levels of TNF are reported to affect the inflammatory cascade [11]. TNFA, produced by monocytes and macrophages, is a potent cytokine with a wide range of proinflammatory activities.…”

Section: Discussionsupporting

confidence: 72%

Investigation of TNFA 308G > A and TNFB 252G > A polymorphisms in genetic susceptibility to migraine

et al. 2009

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We aimed to look for the association of tumor necrosis factor (TNF) gene polymorphisms (TNFA 308G > A, and TNFB 252G > A) in genetic susceptibility to migraine. The pathogenesis of migraine involves many immune-mediated mechanisms in the vascular endothelium. TNF, being a potent immunomodulator and pro-inflammatory cytokine, is suggested to be involved in inflammatory reactions leading to migraine attacks. A total of 216 normotensive migraine patients, 160 tension type headache (TTH) patients and 216 healthy controls (HC) were recruited in the study. The genetic polymorphisms were investigated through SNP association analysis using a matched case control migraine population. Genotyping of TNFA 308G > A polymorphism and TNFB 252G > A was done using ARMS PCR and PCR-RFLP, respectively. A borderline association was observed in TNFA 308GA genotype in migraine patients versus HC (p = 0.043; OR = 1.763; 95% CI = 1.019-3.051). After sub-grouping migraine into migraine with aura (MA) or without aura, significant difference at genotypic (p = 0.015; OR = 2.293; 95% CI = 1.172-4.487) as well as allelic (p = 0.035; OR = 1.955; 95% CI = 1.047-3.651) level was evident. The difference was even more significant in female MA at genotypic (p = 0.006; OR = 2.901; 95% CI = 1.361-6.181) and allelic level (p = 0.017; OR = 2.318; 95% CI = 1.159-4.635) as well as for A allele carriers in MA [p value = 0.020; OR = 2.205 (1.132-4.295)] and female MA (p value = 0.008; OR = 2.741; CI = 1.297-5.792). No association of TNFB252G > A was observed in migraine patients or any subgroups. We did not find any association of TNFA or TNFB gene polymorphisms with TTH. In conclusion, the TNFA 308G > A polymorphism was found to be associated with MA, particularly in females, whereas we could not find any association of TNFB 252G > A polymorphism in genetic susceptibility to migraine on comparing the migraine patients with HC or TTH patients.

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Section: Discussionsupporting

confidence: 72%

Investigation of TNFA 308G > A and TNFB 252G > A polymorphisms in genetic susceptibility to migraine

et al. 2009

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“…Such a frontal cortical dysfunction might interfere with individual autonomic response patterns 40 to potentially stressful situations, disturbing the interactions between cognitive appraisal and general state of health, which, in turn, reflects the interplay between genetic factors, behaviors, and lifestyle choices. 10,41 This mechanism might also be playing a role in other clinical conditions, such as orthostatic intolerance 42 or chronic fatigue, 43 in which subjective symptoms accompany alterations of autonomic regulation.…”

Section: Discussionmentioning

confidence: 99%

Impact of Chronic Psychosocial Stress on Autonomic Cardiovascular Regulation in Otherwise Healthy Subjects

et al. 2005

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Abstract-Elevated psychosocial stress might favor the occurrence of cardiovascular disease; however, mechanisms are incompletely understood. We hypothesized that patients (nϭ126; 44Ϯ1 years of age) referred to an internal medicine clinic because of symptoms related to chronic psychosocial stress would demonstrate signs of autonomic dysregulation compared with controls (nϭ132; 42Ϯ1 years of age). We used autoregressive spectral analysis of RR interval variability to obtain indirect markers of sympathetic and of vagal (respectively, low-frequency and high-frequency components, both expressed in normalized units) oscillatory modulation of sinoatrial node, as well as of sympathetic vasomotor regulation (low-frequency component of systolic arterial pressure variability) and of cardiac baroreflex sensitivity (␣-index

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“…Low zinc concentration is associated with a major risk of cardiovascular diseases and cardiac oxidative damage, and enhances the susceptibility of the heart to oxidative damage leading to cardioischaemia (DiSilvestro 2000). The allele A of the TNF-a -308 G/A polymorphism is coupled with increased production of TNF-a in vitro (Wilson et al 1997) and in vivo (Louis et al 1998;Cipriano et al 2005), with enhanced CRP (Jeanmonod et al 2004) and with low plasma zinc levels . No association of this polymorphism with CAD is found (Koch et al 2001;Gander et al 2004), whereas other investigations reports a relation between -308 TNF-alpha A allele and coronary heart disease (CHD) (Vendrell et al 2003) or unstable angina (Bernard et al 2003), also in obese CAD patients (Padovani et al 2000).…”

Section: Introductionmentioning

confidence: 97%

Involvement of −308 TNF-α and 1267 Hsp70-2 polymorphisms and zinc status in the susceptibility of coronary artery disease (CAD) in old patients

et al. 2006

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Coronary artery disease (CAD) is characterized by an inflammatory status and it represents the major cause of death in elderly. Zinc deficiency and inflammatory genes within major histocompatibility complex (MHC) region are implicated in ischaemic heart diseases. TNF-alpha is present in coronary artery plaques and may provoke plaque instability. Hsp70 plays instead a pro-atherogenic role, via proinflammatory cytokine production, in atherosclerotic lesions contributing to plaque rupture. Contradictory data report the association between -308 TNF-alpha polymorphism and CAD, while no investigations exist on Hsp70-2 gene in CAD. In the current study, we analysed -308 TNF-alpha and 1267 Hsp70-2 polymorphisms and zinc status in 190 healthy old controls and 216 old patients with carotid stenosis subdivided in two groups: the first one 105 patients with CAD (C group), and the second one 111 patients without cardiovascular events (D group). We found a lack of association between -308 TNF-alpha polymorphism and CAD. Conversely, 1267 Hsp70-2 polymorphism was associated with CAD. In particular, significant higher frequency of AB + BB genotypes (B + genotype) was observed in C patients than controls (71.4 vs.56.9%, P = 0.017, odds ratio = 1.898). However, when C patients were subdivided into four subgroups on the basis of presence/absence of 1267B Hsp70-2 and -308A TNF-alpha alleles, B + A + patients showed higher prothrombin activity as well as Hsp70-2, TNF-alpha, IL-6 gene expressions in carotid atheroma when compared to B - A - genotypes. The zinc status (plasma and Zn/Fe ratio in erythrocytes) is not affected by these polymorphisms. However, zinc deficiency is present in CAD condition. In conclusion, 1267 HSP70-2 polymorphism and zinc deficiency, rather than -308 TNF-alpha, are independently associated with CAD. B + A+ and B + A- carriers seem more predisposed to ischaemic events; conversely, B - A- genotype may be considered a protective marker against CAD.

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Elevated Plasma C-Reactive Protein in Chronically Distressed Subjects Who Carry the A Allele of the TNF-α −308 G/A Polymorphism

Cited by 51 publications

References 33 publications

Investigation of TNFA 308G > A and TNFB 252G > A polymorphisms in genetic susceptibility to migraine

Investigation of TNFA 308G > A and TNFB 252G > A polymorphisms in genetic susceptibility to migraine

Impact of Chronic Psychosocial Stress on Autonomic Cardiovascular Regulation in Otherwise Healthy Subjects

Involvement of −308 TNF-α and 1267 Hsp70-2 polymorphisms and zinc status in the susceptibility of coronary artery disease (CAD) in old patients

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