Evaluation of Nonspecific Immunity and Plasma Levels of Interferon-γ, Interleukin-6 and Tumor Necrosis Factor-α in Preeclampsia

Munno, I; Chiechi, Luigi Mario; Lacedra, Giuseppe; Berardesca, C; Patimo, Caterina; Marcuccio, L; Nardelli, Pietro; Loizzi, P

doi:10.3109/08923979909007125

Cited by 20 publications

(21 citation statements)

References 19 publications

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“…Contrary to many other studies (Munno et al, 1999;Omu et al, 1999), we found no evidence that the circulating marker of immune activation, TNF-a, is significantly increased in the serum of women with preeclampsia compared with normal pregnancy. Our results, however, are consistent with the findings of Moodley and Devjee (1998) and Heyl et al (1999).…”

Section: Discussioncontrasting

confidence: 85%

Systemic inflammatory indices in pre-eclampsia and eclampsia

Bowen

Moodley²,

Dutton³

et al. 2001

Journal of Obstetrics and Gynaecology

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The objective of this study was to test the hypothesis that TNF-alpha, TNFp55 receptor and sICAM-1 are markers of immune activation, protective response to concentrations of TNF-alpha and endothelial cell activation, respectively, in pre-eclampsia. In addition, MPO and sL-selectin were selected as blood discriminators of neutrophil activation. This was a cross-sectional study comparing 21 non-pregnant controls, 29 normal pregnant controls, 21 pre-eclamptic and six eclamptic women. Blood concentrations of TNF-alpha, sTNFp55 receptor, sICAM-1, sL-selectin, myeloperoxidase, leucocyte count, neutrophil count, C-reactive protein and gamma-glutamyl transferase were estimated. The neutrophil count was significantly decreased in pre-eclampsia compared with normal pregnancy (9.12+/-0.95 vs. 12.52+/-0.80 x 10(9)/l, P<0.01). Serum concentrations of sL-selectin were significantly higher in non-pregnant controls compared with pregnant controls (P<0.0001), pre-eclampsia (P<0.0001) and eclampsia (P<0.0001). Serum concentrations of TNF-alpha, sTNFp55 receptor, sICAM-1, sL-selectin and MPO were not significantly different in women with pre-eclampsia compared with normal pregnancy. Serum concentrations of TNF-alpha, sTNFp55, sICAM-1, sL-selectin and MPO did not discriminate between normal and pre-eclamptic pregnancies. The high neutrophil count in normal and eclamptic pregnancies and the lack of shedded L-selectin suggests that neutrophil exudation to inflammatory sites was increased in women with an accompanying inflammatory response.

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Section: Discussioncontrasting

confidence: 85%

Systemic inflammatory indices in pre-eclampsia and eclampsia

Bowen

Moodley²,

Dutton³

et al. 2001

Journal of Obstetrics and Gynaecology

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“…There are studies indicating a consistent increase in TNF-a production, 39 others reporting that a part of these patients exhibit Table 2 Genotype frequencies of the TNF-a promoter (À308 G4A), IL6 promoter (À174 G4C), IFN-c intron 1 (+874 A4T), IL10 promoter (À1082 A4G), (À819 C4T), (À592 C4A) and TGF-b1 codon 10 (+869 T4C), codon 25 (+915 G4C) polymorphisms in women with preeclampsia, eclampsia and controls a high TNF levels, 40 whereas some investigators did not detect any change in cytokine levels. 41 These discrepancies have been reported for almost all cytokines. 42 These several conflicting findings could be because of heterogeneity in study designs, definition of phenotype, SNP selection, population diversity and sample size.…”

Section: Discussionmentioning

confidence: 93%

Cytokine gene polymorphisms in preeclampsia and eclampsia

Lima¹,

Sass

Mattar

et al. 2009

Hypertens Res

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The clinical spectrum of preeclampsia (PE) ranges from mild hypertension to severe vasospasm associated with convulsions and multiple organ damage. The biological factors that determine the progression of PE to eclampsia (E) are unknown. Endothelial cell activation seems related to an impaired maternal immune response. The production of cytokines, IL-10 and TGF-b1, is apparently suppressed, and altered IL-2/IL-10 and TNF-a/IL-10 ratios have been reported in preeclamptic cases. The relationship between PE and cytokine gene polymorphism has been studied, but there are few studies that include eclamptic patients. This study aimed at investigating whether polymorphisms in genes, TNF-a promoter (À308 G4A), IL6 promoter (À174 G4C), IFN-c intron 1 (+874 A4T), IL10 promoters (À1082 A4G), (À819 C4T) and (À592 C4A) and TGF-b1 codon 10 (+869 T4C) and codon 25 (+915 G4C) are associated with E and/or PE. Genotyping was carried out in 266 Mulatto women from the northeastern region of Brazil who were referred to a single maternity hospital: 92 with PE, 73 with E and 101 normotensive controls. The v 2 or Fisher's exact tests were used to compare genotype frequencies. Among the six singlenucleotide polymorphisms (SNPs) studied, we found no difference in genotype frequencies between the groups. There was a higher frequency of IFN-c (+874 A) in eclamptic patients in comparison with that in controls. (70.3 vs. 57.8%, respectively; P¼0.02). There were no other significant differences in allelic frequencies between eclamptic, preeclamptic and control groups We found no independent association between any single SNP and PE or E risk in this population of Mulatto women from the northeastern region of Brazil.

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“…41,43,48,49 . As the present study was undertaken in women with established pre-eclampsia, it is not possible to determine whether the altered cytokine levels represent a cause or consequence of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…For individual cytokines, we observed increased TNF-a and IL-6 and reduced IL-10 in the combined pre-eclampsia cohort compared with matched normal pregnancy controls; these are consistent with other published reports. [40][41][42][43][44][45][46] The imbalance between inflammatory and anti-inflammatory cytokines probably contributes to endothelial dysfunction, 47 and is therefore linked with the pathogenesis of preeclampsia…”

Section: Discussionmentioning

confidence: 99%

“…No significant difference was detected in ratios of serum IL-2:IL-10 and IFN-c:IL-10 among study groups (Table S1). For individual cytokines, IL-6, IL-10 and TNF-a varied among groups (Kruskal-Wallis P = 0.0089, 0.0186, 0.0192, respectively), but not IL-2, and IFN-c Kruskal-Wallis P = 0.6221, 0.3034, respectively) Pre-eclampsia (as a single combined group of early-and 35 [19,43] 33 [24,41] 34 [23,41] 33 [24,39] 34 [25,42] 33 [29,43] 32 [21,43] 15 (60) 21 (84) 22 (88) 15 (60) 15 (60 weeks); MAP, mean arterial pressure = diastolic blood pressure + (pulse pressure/3); nIUGR, normotensive intrauterine growth restriction; PET, pre-eclampsia; SGA, small for gestational age.…”

Section: Clinical Characteristicsmentioning

confidence: 99%

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Toll‐like receptors 2 and 4 and the cryopyrin inflammasome in normal pregnancy and pre‐eclampsia

Xie¹,

Hu²,

Turvey

et al. 2009

BJOG

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Objective Pre-eclampsia involves a maternal inflammatory response that differs from both normal pregnancy and normotensive intrauterine growth restriction (IUGR). Our objective was to examine neutrophil Toll-like receptor (TLR), cryopyrin, nuclear factor-jB (NF-jB) subunit and interleukin-1b (IL-1b), and inflammatory cytokine profiles in women with preeclampsia or normotensive IUGR, as well as in normal pregnancy and non-pregnancy controls.Design and method A case-control study was performed. We examined the messenger RNA (mRNA) and protein expressions of TLR4 and TLR2, mRNA levels of cryopyrin, IL-1b, NF-jB subunits p50 and p65, as well as maternal serum inflammatory cytokine profiles (IL-2, IL-6, tumour necrosis factor-a [TNF-a], interferon-c [IFN-c] and IL-10) in women with and without pre-eclampsia using real-time reverse transcription polymerase chain reactions, flow cytometry and multiplex immunoassays.Setting A single tertiary maternity hospital in Vancouver, Canada.Population Women with early-onset pre-eclampsia (<34 weeks of gestation, n = 25), women with late-onset pre-eclampsia ( ‡34 +0 weeks of gestation, n = 25), women with normotensive IUGR (n = 25), women with normal pregnancy (n = 75) and non-pregnancy (n = 25) controls.Results Women with pre-eclampsia (as a single combined group of early-and late-onset, and particularly in women with earlyonset pre-eclampsia) had increased TLR2 and TLR4 mRNA and protein expressions elevated cryopyrin, NF-jB subunit, and IL-1b mRNA expression, and TNF-a:IL-10 and IL-6:IL-10 ratios compared with other groups.Conclusions These data suggest that TLRs and cryopyrin may modulate the innate immune response of the maternal syndrome of pre-eclampsia, and might also trigger the differential inflammatory response existing between early onset pre-eclampsia and normotensive IUGR.

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Evaluation of Nonspecific Immunity and Plasma Levels of Interferon-γ, Interleukin-6 and Tumor Necrosis Factor-α in Preeclampsia

Cited by 20 publications

References 19 publications

Systemic inflammatory indices in pre-eclampsia and eclampsia

Systemic inflammatory indices in pre-eclampsia and eclampsia

Cytokine gene polymorphisms in preeclampsia and eclampsia

Toll‐like receptors 2 and 4 and the cryopyrin inflammasome in normal pregnancy and pre‐eclampsia

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