Research

Monocyte/macrophage and T-cell infiltrates in peritoneum of patients with ovarian cancer or benign pelvic disease

Xipeng Wang¹ , Michael Deavers² , Rebecca Patenia³ , Roland L Bassett Jr⁴ , Peter Mueller⁴ , Qing Ma⁵ , Ena Wang⁶ and Ralph S Freedman³

¹  Department of Obstetrics and Gynecology, Renji Hospital, Shanghai Tiao Tong University, Shanghai, China

²  Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

³  Department of Gynecologic Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

⁴  Department of Biostatistics and Applied Mathematics, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

⁵  Department of Blood and Marrow Transplantation, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA

⁶  Department of Transfusion Medicine, National Institutes of Health, Bethesda, Maryland, USA

author email corresponding author email

Journal of Translational Medicine 2006, 4:30doi:10.1186/1479-5876-4-30

Published:	6 July 2006

Abstract

Background

We previously showed that tumor-free peritoneum of patients with epithelial ovarian cancer (EOC) exhibited enhanced expression of several inflammatory response genes compared to peritoneum of benign disease. Here, we examined peritoneal inflammatory cell patterns to determine their concordance with selected enhanced genes.

Methods

Expression patterns of selected inflammatory genes were mined from our previously published data base. Bilateral pelvic peritoneal and subjacent stromal specimens were obtained from 20 women with EOC and 7 women with benign pelvic conditions. Sections were first stained by indirect immunoperoxidase and numbers of monocytes/macrophages (MO/MA), T cells, B cells, and NK cells counted. Proportions of CD68+ cells and CD3+ cells that coexpressed MO/MA differentiation factors (CD163, CCR1, CXCR8, VCAM1, and phosphorylated cytosolic phospholipase A₂ [pcPLA₂]), which had demonstrated expression in EOC peritoneal samples, were determined by multicolor immunofluorescence.

Results

MO/MA were present on both sides of the pelvic peritoneum in EOC patients, with infiltration of the subjacent stroma and mesothelium. CD68+ MO/MA, the most commonly represented population, and CD3+ T cells were present more often in EOC than in benign pelvic tumors. NK cells, B cells, and granulocytes were rare. CXCL8 (IL-8) and the chemokine receptor CCR1 were coexpressed more frequently on MO/MA than on CD3+ cells contrasting with CD68+/CD163+ cells that coexpressed CXCL8 less often. An important activated enzyme in the eicosanoid pathway, pcPLA₂, was highly expressed on both CD68+ and CD163+ cells. The adherence molecule Vascular Cell Adhesion Molecule-1 (VCAM1) was expressed on CD31+ endothelial cells and on a proportion of CD68+ MO/MA but rarely on CD3+ cells.

Conclusion

The pelvic peritoneum in EOC exhibits a general pattern of chronic inflammation, represented primarily by differentiated MO/MA, and distinct from that in benign conditions concordant with previous profiling results.