Th1/Th2 balance in preeclampsia

Saito, Shigeru; Sakai, Masatoshi

doi:10.1016/s0165-0378(03)00045-7

Cited by 275 publications

(228 citation statements)

References 63 publications

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“…However, both excessive Th1 (pro-inflammatory) and Th2 (anti-inflammatory) cytokine productions have been associated with PE. [3][4][5]34,35 Hence, although we selected only patients with PE, we may have evaluated a heterogeneous population, including women with different cytokine and genetic profiles.…”

Section: Discussionmentioning

confidence: 99%

“…3 Excessive innate activity and a shift toward an inflammatory cytokine profile have been reported in PE. 4,5 Elevated levels of Th-1 cytokines, such as tumor necrosis factor TNF-a, IFN-g and low IL-4 production by phytohemagglutinin-stimulated peripheral blood mononuclear cells have been identified in preeclamptic patients. The production of immunoregulatory 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 placental tissue from preeclamptic cases.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cytokine gene polymorphisms in preeclampsia and eclampsia

Lima¹,

Sass

Mattar

et al. 2009

Hypertens Res

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“…3,4 The systemic inflammatory response involves a rise in the number and activation of leukocytes (monocytes, granulocytes and natural killer cells) with the production of proteases and proinflammatory cytokines leading to T-helper type 1 bias, as well as the activation of endothelial cells, platelets, the coagulation and complement systems and the production of acute-phase proteins. [5][6][7][8] The development of preeclampsia is influenced by both genetic and environmental risk factors, suggesting its multifactorial inheritance. [9][10][11][12][13][14] The a 2 -Heremans-Schmid (a 2 -HS) glycoprotein (fetuin-A, AHSG), the human homolog of bovine fetuin, is an abundant plasma/serum protein synthesized predominantly by hepatocytes.…”

Section: Introductionmentioning

confidence: 99%

Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

et al. 2009

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The purpose of this study was to determine serum a 2 -HS glycoprotein (AHSG) concentration and its diagnostic accuracy in preeclampsia. In this case-control study, the serum C-reactive protein (CRP) and AHSG levels were measured in 93 preeclamptic patients and in 127 healthy pregnant women by immunoturbidimetry and radial immunodiffusion. The serum CRP levels were significantly higher, whereas the serum AHSG concentrations were significantly lower in the preeclamptic group than in the control group (median (25th to 75th percentile), CRP: 6.71 mg l À1 (2.76-12.69) vs. 3.38 mg l À1 (1.69-7.27), respectively; AHSG: 660 lg ml À1 (612-768) vs. 744 lg ml À1 (660-816), respectively; Po0.001 for both). In preeclamptic patients, the serum AHSG concentrations showed significant inverse correlations with systolic blood pressure and serum CRP levels. A low serum AHSG level (p720 lg ml À1 ) was significantly associated with preeclampsia (adjusted odds ratio (95% confidence interval): 3.69 (1.82-7.51); Po0.001). According to the receiver operating characteristic curves, the measurement of serum AHSG concentrations was as accurate as that of serum CRP levels to detect preeclampsia. In conclusion, serum AHSG concentration is decreased and reflects-at least partly-systemic inflammation in preeclampsia.

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“…[17][18][19][20][21] Interestingly, these biological processes are altered in women with preeclampsia. 1,22,23 These observations led us to hypothesize that neutrophil infiltration could affect vascular expression of MMPs and other extracellular matrix proteins, resulting in vascular dysfunction in women with preeclampsia. By using blood vessels from omental fat, we found that MMP-1 is increased in the vasculature of women with preeclampsia compared with those experiencing a healthy pregnancy.…”

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confidence: 99%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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This study was conducted to determine the following: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in systemic vessels of preeclamptic women, (2) whether this increase might be mediated by neutrophils, and (3) whether MMP-1 could be responsible for vascular dysfunction. Omental arteries and plasma were collected from healthy pregnant and preeclamptic women. Omental arteries were evaluated for gene and protein expression of MMP-1, collagen type 1␣, tissue inhibitor of metalloproteinase-1, and vascular reactivity to MMP-1. Gene and protein expression levels were also evaluated in human vascular smooth muscle cells (VSMCs) co-cultured with activated neutrophils, reactive oxygen species, or tumor necrosis factor ␣. Vessel expression of MMP-1 and circulating MMP-1 levels were increased in preeclamptic women, whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regulated or unchanged. In cultured VSMCs, the imbalance in collagen-regulating genes of preeclamptic vessels was reproduced by treatment with neutrophils, tumor necrosis factor ␣, or reactive oxygen species. Chemotaxis studies with cultured cells revealed that MMP-1 promoted recruitment of neutrophils via vascular smooth muscle release of interleukin-8. Furthermore, MMP-1 induced vasoconstriction via protease-activated receptor-1, whose expression was significantly increased in omental arteries of preeclamptic women and in VSMCs co-cultured with neutrophils. Collectively, these findings disclose a novel role for MMP-1 as a mediator of vasoconstriction and vascular dysfunction in preeclampsia.

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Th1/Th2 balance in preeclampsia

Cited by 275 publications

References 63 publications

Cytokine gene polymorphisms in preeclampsia and eclampsia

Cytokine gene polymorphisms in preeclampsia and eclampsia

Preeclampsia is associated with decreased serum α2-HS glycoprotein (fetuin-A) concentration

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

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