Histomorphometric and immunohistochemical analysis of infectious agents, T-cell subpopulations and inflammatory adhesion molecules in placentas from HIV-seropositive pregnant women

Diagnostic Pathology

Lucia de Noronha⁴  Cristina R Cruz²  Larissa LG Silva³  Camilla R Pimentel⁴  Mônica G Santos⁴  Maíra C Mecatti⁴  Augusto O Saito⁴  Karla Abujamra⁴  Camila DA Souza⁴  N Victor Moreschi⁴  Ana PC Martins⁴  Emanuele Baurakiades¹ 

[1] Center of Health and Biological Sciences, Pontifícia Universidade Católica do Paraná, (Imaculada Conceição), Curitiba, (80215-901), Brazil;Pediatric Department, Institute: Universidade Federal do Paraná, (General Carneiro), Curitiba, (80060-900), Brazil;Pathological Anatomy Department, Universidade Federal do Paraná, (General Carneiro), Curitiba, (80060-900), Brazil;Laboratory of Experimental Pathology of Center of Health and Biological Sciences, Pontifícia Universidade Católica do Paraná, (Imaculada Conceição), Curitiba, (80215-901), Brazil

关键词: placenta;    VCAM;    ICAM;    CD8;    CD4;    p24;    HIV;   

Others  :  808220
DOI  :  10.1186/1746-1596-6-101

 received in 2011-05-20, accepted in 2011-10-24,  发布年份 2011

【 摘 要 】

Background

The aim of this study was to compare histomorphometric changes and the results of immunohistochemical tests for VCAM, ICAM-1, CD4 and CD8 in normal placentas from HIV-seropositive pregnant women.

Methods

Samples of normal placentas were divided into 2 groups: healthy HIV-seronegative pregnant women (control group = C = 60) and HIV-seropositive women (experimental group = E = 57). Conventional histological sections were submitted to morphometric analysis and evaluated in terms of the immunohistochemical expression of ICAM-1, VCAM, CD4 and CD8.

Results

The villi in group E were smaller than those in group C. The median for the CD8+ T cell count was higher in group E than in group C (p = 0.03). Immunohistochemical expression of ICAM-1 was observed in 57% of the cases in group E, compared with 21% of those in group C (p = 0.001). There was no difference in VCAM expression or CD4+ cell counts between groups and no correlation between the data for antiretroviral therapy and morphometric or immunohistochemical data.

Conclusions

The morphometric data showed that placentas of HIV-seropositive pregnant women tend to have smaller villi than those of seronegative women. In addition, immunohistochemical testing for infectious agents helped to identify cases that were positive for microorganisms (6/112) that routine pathological examination had failed to detect. The anti-p24 antibody had a limited ability to detect HIV viral protein in this study (2/57). Correlation of immunohistochemical expression of CD8+ T cells and ICAM-1 with the presence of HIV in the placenta revealed that those expressions can act as biomarkers of inflammatory changes. There was no correlation between the data for antiretroviral therapy and morphometric or immunohistochemical data.

【 授权许可】

   
2011 Baurakiades et al; licensee BioMed Central Ltd.

【 参考文献 】

• [1]Ministério da Saúde: Boletim Epidemiológico de AIDS 2004 Ano XVII, 25 a 52 Semanas Epidemiológicas. Brasilia; 2004.
• [2]Marlin R, Nugeyre MT, de Truchis C, et al.: Antigen-Presenting Cells Represent Targets for R5 HIV-1 Infection in the First Trimester Pregnancy Uterine Mucosa. Human Decidua and HIV-1. PLoS One 2009, 4:e5971.
• [3]SheiKh AU, Polliotti BM, Miller RK: Human immunodeficiency virus infection: In situ polymerase chain reaction localization in human placentas after in utero and in vitro infection. Am J Obstet Gynecol 2000, 182:207-213.
• [4]Tripathi V, Verma R, Dinda A, et al.: Differential Expression of RDC1/CXCR7 in the human Placenta. J Clin Immunol 2008, 29:379-86.
• [5]Bogliolo BFG: Patologia Obstétrica. In Patologia Bogliolo. 7th edition. Edited by Guanabara Koogan. Rio de Janeiro; 2006:644-659.
• [6]Villegas-Castrejon H, Paredes-Vivas Y, Flores-Rivera E, et al.: Comparative study of the placenta from HIV+ mothers. Ultrastructural analysis. Ginecol Obstet Mex 1996, 64:167-176.
• [7]Schwartz DA, Sungkarat S, Shaffer N, et al.: Placental abnormalities associated with human immunodeficiency virus type 1 infection and perinatal transmission in Bangkok, Thailand. J Infect Dis 2000, 182:1652-1657.
• [8]Bruch J, Nessmann C: Development of the placenta and viral infections. Path Biol 1992, 40:679-684.
• [9]Anderson VM: The placental barrier to maternal HIV infection. Obstet Gynecol Clin North Am 1997, 24:797-820.
• [10]Lee BN, Ordones N, Popek EJ, et al.: Inflamatory cytokine expression is correlated with the level of human immunodeficiency virus (HIV) transcripts in HIV-infected placental trophoblastic cells. J Virol 1997, 71:3628-35.
• [11]Tscherning-Casper C, Papadogiannakis N, Anvret M, et al.: The trophoblastic epitelial barrier is not infected in full-term placentae of human immunodeficiency virus-seropositive mothers undergoing antiretroviral therapy. J Virol 1999, 73:9673-9678.
• [12]Mattern CFT, Murray K, Jensen A, et al.: Localization of human immunodeficiency virus core antigen in term human placentas. Pediatrics 1992, 89:207-209.
• [13]Menu E, Mbopi-Keou FX, Lagaye S, et al.: Selection of maternal human immunodeficiency virus type 1 variants in human placenta. J Infect Dis 1999, 179:44-51.
• [14]Haytlick SJ: The Intercellular Adhesion Molecule. Immunologic Research 1998, 17:313-327.
• [15]Anderson ME, Siahaan TJ: Mechanism of Binding and Internalization of ICAM-1-Derived Cyclic Peptides by LFA-1 on the Surface of T Cells: A Potential Method for Targeted Drug Delivery. Pharm Res 2003, 20:1523-1532.
• [16]Legrand FA, Nixon DF, Loo CP, et al.: Strong HIV-1-Specific T Cell Responses in HIV-1-ExposedUninfected Infants and Neonates Revealed after Regulatory T Cell Removal. Plos One 2006, 1:e102.
• [17]Toth FD, Mosborg-Petersen P, Kiss J, et al.: Interactions between Human Immunodeficiency Virus Type 1 and Human Cytomegalovirus in Human Term Syncytiotrophoblast Cells Coinfected with Both Viruses. J Virol 1995, 69:2223-2232.
• [18]Jung-Sun K: Involvement of Hofbauer cells and maternal T cells in villitis of unknown etiology. Histopathology 2008, 52:457-464.
• [19]Farquhar C, Stewar J: The role of infant immune responses and genetic factors in preventing HIV-1 acquisition and disease progression. Clin Exp Immunol 2003, 134:367-377.
• [20]Fear WR, Kesson AM, Naif H, et al.: Differential tropism and chemokine receptor expression of human immunodeficiency virus type 1 in neonatal monocytes, monocyte-derived macrophages, and placental macrophages. J Virol 1998, 72:1334-1344.
• [21]Schwartz RH: A cell culture model for T lymphocite clonal anergy. Science 1998, 1349:1480.