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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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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