Role of immunoreactions and mast cells in pathogenesis of human endometriosis -morphologic study and gene expression analysis-

Ryo Konno, Konno R, Yamada-Okabe H, Hisafumi Yamada-Okabe, Hisafumi Yamada‐Okabe, Fujiwara H, Hiroyuki Fujiwara, Ichiro Uchiide, Uchiide I, Hiroaki Shibahara, Shibahara H, Ohwada M, Michitaka Ohwada, Ihara T, Tomomi Ihara, Masao Sugamata, Sugamata M, Mitsuaki Suzuki, Suzuki M
Human cell · 2003 · vol. 16(3) , pp. 141–149 · doi:10.1111/j.1749-0774.2003.tb00146.x · PMID:15005245 · W2085438111
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Morphological and gene expression analysis revealed mast cell infiltration and upregulated inflammatory and tissue remodeling gene expression in ovarian endometriotic lesions, suggesting their role in fibrosis and adhesions.

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Abstract

Study objectivesTo investigate the pathophysiology of human endometriosis, we examined by morphological and molecular biological methods.MethodsSamples of ovarian endometriosis and normal ovarian tissues were obtained laparoscopically after informed consent. A morphological study by toluidine blue staining, immunohistochemistry of c-kit and electron microscopy demonstrated the localization of mast cells in the stromal lesions of endometriosis. Oligonucleotide microarrays were used for gene expression analysis.ResultsInfiltration of numerous mast cells and development of fibrosis was observed throughout the stromal lesions. Gene expression analysis by oligonucleotide microarrays indicated inflammatory immunoreactions in the lesions. Expressions of the FCER1G and PGDS, which are considered to be mast cell-specific genes, were upregulated in the ovarian endometriotic lesions as compared to the normal ovarian tissues. Furthermore, expressions of genes associated with immunological inflammation, such as IL-8, GRO1, GRO2, CXCR4, MCP1, and those related to tissue remodeling (MMP, COL4A2, and COL5A2) were also higher in endometriotic lesions than in the normal ovarian tissue.ConclusionsThus it is likely that mast cells and their related inflammatory immunoreactions via chemokines play important roles in producing fibrosis and adhesions in endometriotic lesions.
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Abstract

Study objectives To investigate the pathophysiology of human endometriosis, we examined by morphological and molecular biological methods.

Methods

Samples of ovarian endometriosis and normal ovarian tissues were obtained laparoscopically after informed consent. A morphological study by toluidine blue staining, immunohistochemistry of c-kit and electron microscopy demonstrated the localization of mast cells in the stromal lesions of endometriosis. Oligonucleotide microarrays were used for gene expression analysis.

Results

Infiltration of numerous mast cells and development of fibrosis was observed throughout the stromal lesions. Gene expression analysis by oligonucleotide microarrays indicated inflammatory immunoreactions in the lesions. Expressions of the FCERlG and PGDS, which are considered to be mast cell-specific genes, were upregulated in the ovarian endometriotic lesions as compared to the normal ovarian tissues. Furthermore, expressions of genes associated with immunological inflammation, such as IL-8, GRO1, GRO2, CXCR4, MCP1, and those related to tissue remodeling (MMP, COLAA2, and COL5A2) were also higher in endometriotic lesions than in the normal ovarian tissue.

Conclusions

Thus it is likely that mast cells and their related inflammatory immunoreactions via chemokines play important roles in producing fibrosis and adhesions in endometriotic lesions. Similar content being viewed by others

Reference

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Role of immunoreactions and mast cells in pathogenesis of human endometriosis-morphologic study and gene expression analysis-. Hum Cell 16, 141–149 (2003). https://doi.org/10.1111/j.1749-0774.2003.tb00146.x Received: Accepted: Published: Issue date: DOI: https://doi.org/10.1111/j.1749-0774.2003.tb00146.x

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endometriosis

MeSH descriptors

Chemokines Endometriosis Mast Cells Ovarian Diseases Proto-Oncogene Proteins c-kit Chemokines Endometriosis Endometriosis Endometriosis Endometriosis Female Gene Expression Regulation, Neoplastic Humans Immunohistochemistry Inflammation Inflammation Inflammation Mast Cells Mast Cells Microscopy, Electron

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