Inflammation by Breast Implants and Adenocarcinoma: Not Always a Bad Company

Monia Orciani, Giulia Sorgentoni, Fabiola Olivieri, Monica Mattioli-Belmonte, Giovanni Di Benedetto, Roberto Di Primio

Research output: Contribution to journalArticle

Abstract

BACKGROUND: Inflammation and tumor are now an inseparable binomial. Inflammation may also derive by the use of breast implants followed by the formation of a periprosthetic capsule. It is known that tumor cells, in an inflamed microenvironment, can profit by the paracrine effect exerted also by mesenchymal stem cells (MSCs). Here we evaluated the role of inflammation on the immunobiology of MSCs before and after cocultures with cells derived from breast adenocarcinoma.

METHODS: MSCs derived from both inflamed (I-MSCs) and control (C-MSCs) tissues were isolated and cocultured with MCF7 cells derived from breast adenocarcinoma. Before and after cocultures, the proliferation rate of MCF7 cells and the expression/secretion of cytokines related to inflammation were tested.

RESULTS: Before cocultures, higher levels of cytokine related to chronic inflammation were detected in I-MSCs than in C-MSCs. After cocultures with MCF7, C- and I-MSCs show a variation in cytokine production. In detail, IL-2, IL-4, IL-5, IL-10, IL-13, TGF-β and G-CSF were decreased, whereas IL-6, IL-12, IFN-γ, and IL-17 were oversecreted. Proliferation of MCF7 was significantly increased after cocultures with I-MSCs.

CONCLUSIONS: Inflammation at the site of origin of MSCs affects their immunobiology. Even if tumor cells increased their proliferation rate after cocultures with I-MSCs, the analysis of the cytokines, known to play a role in the interference of tumor cells with the host immune system, absolves completely the breast implants from the insult to enforce the risk of adenocarcinoma.

Original languageEnglish
Pages (from-to)286-292
Number of pages7
JournalClinical Breast Cancer
Volume17
Issue number4
DOIs
Publication statusPublished - Jul 2018

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Breast Implants
Mesenchymal Stromal Cells
Adenocarcinoma
Inflammation
Coculture Techniques
Cytokines
MCF-7 Cells
Neoplasms
Breast
Interleukin-13
Interleukin-17
Interleukin-5
Granulocyte Colony-Stimulating Factor
Interleukin-12
Interleukin-4
Interleukin-10
Capsules
Interleukin-2
Immune System
Interleukin-6

Keywords

  • Journal Article

Cite this

Orciani, M., Sorgentoni, G., Olivieri, F., Mattioli-Belmonte, M., Di Benedetto, G., & Di Primio, R. (2018). Inflammation by Breast Implants and Adenocarcinoma: Not Always a Bad Company. Clinical Breast Cancer, 17(4), 286-292. https://doi.org/10.1016/j.clbc.2017.01.001

Inflammation by Breast Implants and Adenocarcinoma : Not Always a Bad Company. / Orciani, Monia; Sorgentoni, Giulia; Olivieri, Fabiola; Mattioli-Belmonte, Monica; Di Benedetto, Giovanni; Di Primio, Roberto.

In: Clinical Breast Cancer, Vol. 17, No. 4, 07.2018, p. 286-292.

Research output: Contribution to journalArticle

Orciani, M, Sorgentoni, G, Olivieri, F, Mattioli-Belmonte, M, Di Benedetto, G & Di Primio, R 2018, 'Inflammation by Breast Implants and Adenocarcinoma: Not Always a Bad Company', Clinical Breast Cancer, vol. 17, no. 4, pp. 286-292. https://doi.org/10.1016/j.clbc.2017.01.001
Orciani M, Sorgentoni G, Olivieri F, Mattioli-Belmonte M, Di Benedetto G, Di Primio R. Inflammation by Breast Implants and Adenocarcinoma: Not Always a Bad Company. Clinical Breast Cancer. 2018 Jul;17(4):286-292. https://doi.org/10.1016/j.clbc.2017.01.001
Orciani, Monia ; Sorgentoni, Giulia ; Olivieri, Fabiola ; Mattioli-Belmonte, Monica ; Di Benedetto, Giovanni ; Di Primio, Roberto. / Inflammation by Breast Implants and Adenocarcinoma : Not Always a Bad Company. In: Clinical Breast Cancer. 2018 ; Vol. 17, No. 4. pp. 286-292.
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AU - Orciani, Monia

AU - Sorgentoni, Giulia

AU - Olivieri, Fabiola

AU - Mattioli-Belmonte, Monica

AU - Di Benedetto, Giovanni

AU - Di Primio, Roberto

N1 - Copyright © 2017 Elsevier Inc. All rights reserved.

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N2 - BACKGROUND: Inflammation and tumor are now an inseparable binomial. Inflammation may also derive by the use of breast implants followed by the formation of a periprosthetic capsule. It is known that tumor cells, in an inflamed microenvironment, can profit by the paracrine effect exerted also by mesenchymal stem cells (MSCs). Here we evaluated the role of inflammation on the immunobiology of MSCs before and after cocultures with cells derived from breast adenocarcinoma.METHODS: MSCs derived from both inflamed (I-MSCs) and control (C-MSCs) tissues were isolated and cocultured with MCF7 cells derived from breast adenocarcinoma. Before and after cocultures, the proliferation rate of MCF7 cells and the expression/secretion of cytokines related to inflammation were tested.RESULTS: Before cocultures, higher levels of cytokine related to chronic inflammation were detected in I-MSCs than in C-MSCs. After cocultures with MCF7, C- and I-MSCs show a variation in cytokine production. In detail, IL-2, IL-4, IL-5, IL-10, IL-13, TGF-β and G-CSF were decreased, whereas IL-6, IL-12, IFN-γ, and IL-17 were oversecreted. Proliferation of MCF7 was significantly increased after cocultures with I-MSCs.CONCLUSIONS: Inflammation at the site of origin of MSCs affects their immunobiology. Even if tumor cells increased their proliferation rate after cocultures with I-MSCs, the analysis of the cytokines, known to play a role in the interference of tumor cells with the host immune system, absolves completely the breast implants from the insult to enforce the risk of adenocarcinoma.

AB - BACKGROUND: Inflammation and tumor are now an inseparable binomial. Inflammation may also derive by the use of breast implants followed by the formation of a periprosthetic capsule. It is known that tumor cells, in an inflamed microenvironment, can profit by the paracrine effect exerted also by mesenchymal stem cells (MSCs). Here we evaluated the role of inflammation on the immunobiology of MSCs before and after cocultures with cells derived from breast adenocarcinoma.METHODS: MSCs derived from both inflamed (I-MSCs) and control (C-MSCs) tissues were isolated and cocultured with MCF7 cells derived from breast adenocarcinoma. Before and after cocultures, the proliferation rate of MCF7 cells and the expression/secretion of cytokines related to inflammation were tested.RESULTS: Before cocultures, higher levels of cytokine related to chronic inflammation were detected in I-MSCs than in C-MSCs. After cocultures with MCF7, C- and I-MSCs show a variation in cytokine production. In detail, IL-2, IL-4, IL-5, IL-10, IL-13, TGF-β and G-CSF were decreased, whereas IL-6, IL-12, IFN-γ, and IL-17 were oversecreted. Proliferation of MCF7 was significantly increased after cocultures with I-MSCs.CONCLUSIONS: Inflammation at the site of origin of MSCs affects their immunobiology. Even if tumor cells increased their proliferation rate after cocultures with I-MSCs, the analysis of the cytokines, known to play a role in the interference of tumor cells with the host immune system, absolves completely the breast implants from the insult to enforce the risk of adenocarcinoma.

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