Is the immunohistochemical study of the inflammatory infiltrate helpful in distinguishing villitis of unknown etiology from non-specific infection villitis?

Brito, Hélio Henrique de Araújo; Juliano, Priscila Bianchi; Altemani, Carlos Alberto Carrasco; Altemani, Albina

doi:10.1016/j.placenta.2004.10.012

Cited by 24 publications

(15 citation statements)

References 10 publications

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“…20,21 Many of the histopathological changes found in viral infections, with or without stillbirth are non-specific, 20,21 and not useful in distinguishing infections from other causes of fetal damage. 143 Consistent with this, many laboratories detect CMV, parvovirus B19 and other viruses in autopsy tissue from stillborn babies, and placental tissue from healthy babies, respectively. 58 Examination of data from in situ PCR (ISPCR) and immunohistochemistry (IHC) have to date shown:…”

Section: Placental and Fetal Histopathology In Virus Infected Stillbimentioning

confidence: 66%

Viruses and other infections in stillbirth: what is the evidence and what should we be doing?

et al. 2008

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Section: Placental and Fetal Histopathology In Virus Infected Stillbimentioning

confidence: 66%

Viruses and other infections in stillbirth: what is the evidence and what should we be doing?

et al. 2008

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“…Other more common causes of granulomatous inflammation such as mycobacterial and fungal infections do not cause chronic villitis. Lymphocytes in VUE are almost exclusively T cells with CD8 positivity predominating over CD4 in most cases (CD4/CD8 ratio range, 0.1-0.5) [18][19][20]. Macrophages are CD68-and HAM 56-positive, but generally Mac387-negative.…”

Section: Pathologymentioning

confidence: 99%

“…Although one would expect both a fetal and maternal response to such exogenous antigens, the immaturity of the fetal immune system may result in predominance of the latter [37,[49][50][51][52]. In fact, several studies have shown that maternal CD8-positive T lymphocytes are prominently represented in the inflammatory infiltrate associated with placental syphilis, toxoplasmosis, and trypanosomiasis [18,20].…”

Section: Target Antigensmentioning

confidence: 99%

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

2007

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“…VUE, an enigmatic and destructive inflammatory lesion, involves the villous placenta and is characterized by infiltration of predominantly CD8 + maternal T cells into the chorionic villi (5,6). VUE is a relatively common lesion found in 5–15% of term placentas, and it is associated with intrauterine fetal growth restriction, fetal death, and a wide range of perinatal morbidity (7–9).…”

Section: Introductionmentioning

confidence: 99%

Villitis of Unknown Etiology Is Associated with a Distinct Pattern of Chemokine Up-Regulation in the Feto-Maternal and Placental Compartments: Implications for Conjoint Maternal Allograft Rejection and Maternal Anti-Fetal Graft-versus-Host Disease

Kim

Romero

Kim

et al. 2009

The Journal of Immunology

177

175

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The co-presence of histoincompatible fetal and maternal cells is a characteristic of human placental inflammation. Villitis of unknown etiology (VUE), a destructive inflammatory lesion of villous placenta, is characterized by participation of Hofbauer cells (placental macrophages) and maternal T cells. In contrast to acute chorioamnionitis of infection-related origin, the fundamental immunopathology of VUE is unknown. This study was performed to investigate the placental transcriptome of VUE and to determine whether VUE is associated with systemic maternal and/or fetal inflammatory response(s). Comparison of the transcriptome between term placentas without and with VUE revealed differential expression of 206 genes associated with pathways related to immune response. The mRNA expression of a subset of chemokines and their receptors (CXCL9, CXCL10, CXCL11, CXCL13, CCL4, CCL5, CXCR3, CCR5) was higher in VUE placentas than in normal placentas (p < 0.05). Analysis of blood cell mRNA showed a higher expression of CXCL9 and CXCL13 in the mother, and CXCL11 and CXCL13 in the fetus of VUE cases (p < 0.05). The median concentrations of CXCL9, CXCL10, and CXCL11 in maternal and fetal plasma were higher in VUE (p < 0.05). Comparison of preterm cases without and with acute chorioamnionitis revealed elevated CXCL9, CXCL10, CXCL11, and CXCL13 concentrations in fetal plasma (p < 0.05), but not in maternal plasma with chorioamnionitis. We report for the first time the placental transcriptome of VUE. A systemic derangement of CXC chemokines in maternal and fetal circulation distinguishes VUE from acute chorioamnionitis. We propose that VUE be a unique state combining maternal allograft rejection and maternal antifetal graft-vs-host disease mechanisms.

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Is the immunohistochemical study of the inflammatory infiltrate helpful in distinguishing villitis of unknown etiology from non-specific infection villitis?

Cited by 24 publications

References 10 publications

Viruses and other infections in stillbirth: what is the evidence and what should we be doing?

Viruses and other infections in stillbirth: what is the evidence and what should we be doing?

Villitis of unknown etiology: noninfectious chronic villitis in the placenta

Villitis of Unknown Etiology Is Associated with a Distinct Pattern of Chemokine Up-Regulation in the Feto-Maternal and Placental Compartments: Implications for Conjoint Maternal Allograft Rejection and Maternal Anti-Fetal Graft-versus-Host Disease

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