Cell mediated immune responses through TLR4 prevents DMBA-induced mammary carcinogenesis in mice
Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR‐4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient...
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| Published in: | International journal of cancer Vol. 130; no. 4; pp. 765 - 774 |
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| Abstract | Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR‐4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12‐dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL‐17 and lower levels of IFN‐γ relative to WT mice. IL‐12 secreted by CD11c+ cells was higher in WT mice, whereas greater amounts of IL‐23 were produced by CD11c+ cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)‐2 and MMP‐9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell‐mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors. |
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| AbstractList | Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR‐4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12‐dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL‐17 and lower levels of IFN‐γ relative to WT mice. IL‐12 secreted by CD11c+ cells was higher in WT mice, whereas greater amounts of IL‐23 were produced by CD11c+ cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)‐2 and MMP‐9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell‐mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors. Toll-like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR-4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL-17 and lower levels of IFN-[gamma] relative to WT mice. IL-12 secreted by CD11c+ cells was higher in WT mice, whereas greater amounts of IL-23 were produced by CD11c+ cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)-2 and MMP-9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell-mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors. [PUBLICATION ABSTRACT] Abstract Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR‐4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12‐dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL‐17 and lower levels of IFN‐γ relative to WT mice. IL‐12 secreted by CD11c + cells was higher in WT mice, whereas greater amounts of IL‐23 were produced by CD11c + cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)‐2 and MMP‐9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell‐mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors. Toll-like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR-4 (TLR4) in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL-17 and lower levels of IFN- gamma relative to WT mice. IL-12 secreted by CD11c super(+) cells was higher in WT mice, whereas greater amounts of IL-23 were produced by CD11c super(+) cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis [matrix metalloproteinases (MMP)-2 and MMP-9, CD31 and vascular endothelial growth factor] were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell-mediated immune response may, therefore, prove to be beneficial in the prevention of mammary tumors. Toll like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have been associated with activation of those pathways. To determine the role of TLR4 in mammary carcinogenesis, we subjected TLR4 deficient and wild type (WT) mice to oral gavage with carcinogenic polyaromatic hydrocarbon 7, 12-dimethylbenz(a)anthracene (DMBA). TLR4 deficient mice developed more tumors relative to the WT mice. T cells of TLR4 deficient mice produced elevated levels of IL-17 and lower levels of IFN-γ relative to WT mice. IL-12 secreted by CD11c+ cells was higher in WT mice whereas greater amounts of IL-23 were produced by CD11c+ cells from TLR4 deficient mice. Moreover, there was higher incidence of regulatory T cells in TLR4 deficient mice than WT mice. Similarly, various markers of angiogenesis (MMP-2 and MMP-9, CD31, and VEGF) were highly expressed in tumors from TLR4 deficient mice than WT mice. The results of this study indicate that TLR4 plays an important role in the prevention of DMBA induced mouse mammary tumorigenesis and efforts to divert the cell-mediated immune response may therefore prove to be beneficial in the prevention of mammary tumors. |
| Author | Nasti, Tahseen H. Kapadia, Akash D. Naseemuddin, Mohammed Yusuf, Nabiha Ghandhi, Jennifer L. Iqbal, Aneeqa |
| AuthorAffiliation | 3 Comprehensive Cancer Center, University of Alabama at Birmingham, AL 1 Department of Dermatology, University of Alabama at Birmingham, AL 2 Veteran Affairs Medical Center, Birmingham, University of Alabama at Birmingham, AL |
| AuthorAffiliation_xml | – name: 1 Department of Dermatology, University of Alabama at Birmingham, AL – name: 2 Veteran Affairs Medical Center, Birmingham, University of Alabama at Birmingham, AL – name: 3 Comprehensive Cancer Center, University of Alabama at Birmingham, AL |
| Author_xml | – sequence: 1 givenname: Mohammed surname: Naseemuddin fullname: Naseemuddin, Mohammed organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL – sequence: 2 givenname: Aneeqa surname: Iqbal fullname: Iqbal, Aneeqa organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL – sequence: 3 givenname: Tahseen H. surname: Nasti fullname: Nasti, Tahseen H. organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL – sequence: 4 givenname: Jennifer L. surname: Ghandhi fullname: Ghandhi, Jennifer L. organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL – sequence: 5 givenname: Akash D. surname: Kapadia fullname: Kapadia, Akash D. organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL – sequence: 6 givenname: Nabiha surname: Yusuf fullname: Yusuf, Nabiha email: nabiha@uab.edu organization: Department of Dermatology and Skin Diseases Research Center, University of Alabama at Birmingham, Birmingham, AL |
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| Keywords | Breast disease Toll like receptor 4 chemical carcinogenesis Rodentia Breast cancer Cellular immunity Malignant tumor Carcinogenesis Prevention Mammary gland diseases Carcinogen Vertebrata Mammalia Cancerology Mouse Animal 7,12-dimethylbenz(a)anthracene toll-like receptor 4 Cancer |
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| Snippet | Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have... Toll-like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have... Abstract Toll‐like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals... Toll like receptors (TLRs) activate signals that are critically involved in the initiation of adaptive immune responses and many tumorigenic chemicals have... |
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| SubjectTerms | 12-dimethylbenz(a)anthracene 7,12‐dimethylbenz(a)anthracene 9,10-Dimethyl-1,2-benzanthracene Animals Biological and medical sciences breast cancer Cancer chemical carcinogenesis Female Genes Gynecology. Andrology. Obstetrics Interferon-gamma - analysis Interleukin-12 - analysis Interleukin-17 - analysis Interleukin-23 - analysis Mammary gland diseases Mammary Neoplasms, Experimental - blood supply Mammary Neoplasms, Experimental - chemically induced Mammary Neoplasms, Experimental - immunology Mammary Neoplasms, Experimental - pathology Medical research Medical sciences Mice Mice, Inbred C3H Neovascularization, Pathologic - etiology Rodents T-Lymphocytes, Regulatory - immunology toll-like receptor 4 Toll-Like Receptor 4 - physiology Transforming Growth Factor beta - physiology Tumors |
| Title | Cell mediated immune responses through TLR4 prevents DMBA-induced mammary carcinogenesis in mice |
| URI | https://api.istex.fr/ark:/67375/WNG-FMLQX7X9-C/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fijc.26100 https://www.ncbi.nlm.nih.gov/pubmed/21455984 https://www.proquest.com/docview/1544960352 https://search.proquest.com/docview/1566831377 https://pubmed.ncbi.nlm.nih.gov/PMC3760716 |
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