Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer

Colitis-associated colorectal cancer (CRC) development has been shown to be related to chronically enhanced inflammation. Macrophage migration inhibitory factor (MIF) is an inflammatory mediator that favors inflammatory cytokine production and has chemotactic properties for the recruitment of macrop...

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Main Authors: Thalia Pacheco-Fernández, Imelda Juárez-Avelar, Oscar Illescas, Luis I. Terrazas, Rogelio Hernández-Pando, Carlos Pérez-Plasencia, Emma B. Gutiérrez-Cirlos, Federico Ávila-Moreno, Yolanda I. Chirino, José Luis Reyes, Vilma Maldonado, Miriam Rodriguez-Sosa
Format: Article
Language:English
Published: Hindawi Limited 2019-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2019/2056085
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spelling doaj-1ccb04a4c5f840b5a9e5cfb0080a49352020-11-25T02:03:07ZengHindawi LimitedMediators of Inflammation0962-93511466-18612019-01-01201910.1155/2019/20560852056085Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal CancerThalia Pacheco-Fernández0Imelda Juárez-Avelar1Oscar Illescas2Luis I. Terrazas3Rogelio Hernández-Pando4Carlos Pérez-Plasencia5Emma B. Gutiérrez-Cirlos6Federico Ávila-Moreno7Yolanda I. Chirino8José Luis Reyes9Vilma Maldonado10Miriam Rodriguez-Sosa11Biomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoExperimental Pathology Section, National Institute of Medical Sciences and Nutrition “Salvador Zubirán”, Tlalpan, C.P. 14000 Mexico city, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoEpigenetics, National Institute of Genomic Medicine, Tlalpan, C.P 14610 Mexico city, MexicoBiomedicine Unit, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México (UNAM), Tlalnepantla C.P. 54090, MexicoColitis-associated colorectal cancer (CRC) development has been shown to be related to chronically enhanced inflammation. Macrophage migration inhibitory factor (MIF) is an inflammatory mediator that favors inflammatory cytokine production and has chemotactic properties for the recruitment of macrophages (Møs) and T cells. Here, we investigated the role of MIF in the inflammatory response and recruitment of immune cells in a murine model of chemical carcinogenesis to establish the impact of MIF on CRC genesis and malignancy. We used BALB/c MIF-knockout (MIF-/-) and wild-type (WT) mice to develop CRC by administering intraperitoneal (i.p.) azoxymethane and dextran sodium sulfate in drinking water. Greater tumor burdens were observed in MIF-/- mice than in WT mice. Tumors from MIF-/- mice were histologically identified to be more aggressive than tumors from WT mice. The localization of MIF suggests that it is also involved in cell differentiation. The relative gene expression of il-17, measured by real-time PCR, was higher in MIF-/- CRC mice, compared to the WT CRC and healthy MIF-/- mice. Importantly, compared to the WT intestinal epithelium, lower percentages of tumor-associated Møs were found in the MIF-/- intestinal epithelium. These results suggest that MIF plays a role in controlling the initial development of CRC by attracting Møs to the tumor, which is a condition that favors the initial antitumor responses.http://dx.doi.org/10.1155/2019/2056085
collection DOAJ
language English
format Article
sources DOAJ
author Thalia Pacheco-Fernández
Imelda Juárez-Avelar
Oscar Illescas
Luis I. Terrazas
Rogelio Hernández-Pando
Carlos Pérez-Plasencia
Emma B. Gutiérrez-Cirlos
Federico Ávila-Moreno
Yolanda I. Chirino
José Luis Reyes
Vilma Maldonado
Miriam Rodriguez-Sosa
spellingShingle Thalia Pacheco-Fernández
Imelda Juárez-Avelar
Oscar Illescas
Luis I. Terrazas
Rogelio Hernández-Pando
Carlos Pérez-Plasencia
Emma B. Gutiérrez-Cirlos
Federico Ávila-Moreno
Yolanda I. Chirino
José Luis Reyes
Vilma Maldonado
Miriam Rodriguez-Sosa
Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
Mediators of Inflammation
author_facet Thalia Pacheco-Fernández
Imelda Juárez-Avelar
Oscar Illescas
Luis I. Terrazas
Rogelio Hernández-Pando
Carlos Pérez-Plasencia
Emma B. Gutiérrez-Cirlos
Federico Ávila-Moreno
Yolanda I. Chirino
José Luis Reyes
Vilma Maldonado
Miriam Rodriguez-Sosa
author_sort Thalia Pacheco-Fernández
title Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
title_short Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
title_full Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
title_fullStr Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
title_full_unstemmed Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer
title_sort macrophage migration inhibitory factor promotes the interaction between the tumor, macrophages, and t cells to regulate the progression of chemically induced colitis-associated colorectal cancer
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2019-01-01
description Colitis-associated colorectal cancer (CRC) development has been shown to be related to chronically enhanced inflammation. Macrophage migration inhibitory factor (MIF) is an inflammatory mediator that favors inflammatory cytokine production and has chemotactic properties for the recruitment of macrophages (Møs) and T cells. Here, we investigated the role of MIF in the inflammatory response and recruitment of immune cells in a murine model of chemical carcinogenesis to establish the impact of MIF on CRC genesis and malignancy. We used BALB/c MIF-knockout (MIF-/-) and wild-type (WT) mice to develop CRC by administering intraperitoneal (i.p.) azoxymethane and dextran sodium sulfate in drinking water. Greater tumor burdens were observed in MIF-/- mice than in WT mice. Tumors from MIF-/- mice were histologically identified to be more aggressive than tumors from WT mice. The localization of MIF suggests that it is also involved in cell differentiation. The relative gene expression of il-17, measured by real-time PCR, was higher in MIF-/- CRC mice, compared to the WT CRC and healthy MIF-/- mice. Importantly, compared to the WT intestinal epithelium, lower percentages of tumor-associated Møs were found in the MIF-/- intestinal epithelium. These results suggest that MIF plays a role in controlling the initial development of CRC by attracting Møs to the tumor, which is a condition that favors the initial antitumor responses.
url http://dx.doi.org/10.1155/2019/2056085
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