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      High-concentrate feeding upregulates the expression of inflammation-related genes in the ruminal epithelium of dairy cattle

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          Abstract

          Background

          The objective of this study was to characterize the mRNA expression profile related to rumen epithelial inflammation through the in vivo and in vitro experiments. In the in vivo experiment, rumen papillae were collected from four dairy cows adapted to either a 40 % (LC) or 70 % (HC) concentrate feeds for microarray analysis.

          Results

          Results showed that 245 differentially expressed genes (DEGs) were detected in the cows fed the HC relative to the LC diet. The DEGs were first annotated, and results revealed that the expression of inflammation-related genes, including IL-1β, IL-2, IL-22, CCL19, CCL8, CX3CR1, CXCL6, INHBE, LEPR, PRL, and TNFRSF9 found in the cytokine-cytokine receptor pathway were up-regulated in the HC-fed cows, indicating local inflammation in the rumen epithelium was triggered. The expression of IL-1β, IL-2, and IL-6 was further validated by qRT-PCR. To demonstrate whether there were relationships between cytokine mRNA expression and ruminal factors (pH and LPS), the isolated ruminal epithelial cells were cultured in vitro. Results showed that the mRNA expression of IL-1β, IL-2, IL-6, and IL-8 increased after the LPS treatment, while low-pH treatment elevated the mRNA expression of TNF-α, suggesting that low-pH coupled with higher levels of LPS in rumen of cows fed the HC may be mainly responsible for the triggered local ruminal inflammation.

          Conclusions

          Our results indicate that ruminal local inflammation response might be triggered during HC feeding, and these findings also enhance the knowledge of rumen epithelial adaptation to HC at the molecular level.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s40104-016-0100-1) contains supplementary material, which is available to authorized users.

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          Most cited references45

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          Gene Ontology: tool for the unification of biology

          Genomic sequencing has made it clear that a large fraction of the genes specifying the core biological functions are shared by all eukaryotes. Knowledge of the biological role of such shared proteins in one organism can often be transferred to other organisms. The goal of the Gene Ontology Consortium is to produce a dynamic, controlled vocabulary that can be applied to all eukaryotes even as knowledge of gene and protein roles in cells is accumulating and changing. To this end, three independent ontologies accessible on the World-Wide Web (http://www.geneontology.org) are being constructed: biological process, molecular function and cellular component.
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            Inflammation in wound repair: molecular and cellular mechanisms.

            In post-natal life the inflammatory response is an inevitable consequence of tissue injury. Experimental studies established the dogma that inflammation is essential to the establishment of cutaneous homeostasis following injury, and in recent years information about specific subsets of inflammatory cell lineages and the cytokine network orchestrating inflammation associated with tissue repair has increased. Recently, this dogma has been challenged, and reports have raised questions on the validity of the essential prerequisite of inflammation for efficient tissue repair. Indeed, in experimental models of repair, inflammation has been shown to delay healing and to result in increased scarring. Furthermore, chronic inflammation, a hallmark of the non-healing wound, predisposes tissue to cancer development. Thus, a more detailed understanding in mechanisms controlling the inflammatory response during repair and how inflammation directs the outcome of the healing process will serve as a significant milestone in the therapy of pathological tissue repair. In this paper, we review cellular and molecular mechanisms controlling inflammation in cutaneous tissue repair and provide a rationale for targeting the inflammatory phase in order to modulate the outcome of the healing response.
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              Interleukins, from 1 to 37, and interferon-γ: receptors, functions, and roles in diseases.

              Advancing our understanding of mechanisms of immune regulation in allergy, asthma, autoimmune diseases, tumor development, organ transplantation, and chronic infections could lead to effective and targeted therapies. Subsets of immune and inflammatory cells interact via ILs and IFNs; reciprocal regulation and counter balance among T(h) and regulatory T cells, as well as subsets of B cells, offer opportunities for immune interventions. Here, we review current knowledge about ILs 1 to 37 and IFN-γ. Our understanding of the effects of ILs has greatly increased since the discoveries of monocyte IL (called IL-1) and lymphocyte IL (called IL-2); more than 40 cytokines are now designated as ILs. Studies of transgenic or knockout mice with altered expression of these cytokines or their receptors and analyses of mutations and polymorphisms in human genes that encode these products have provided important information about IL and IFN functions. We discuss their signaling pathways, cellular sources, targets, roles in immune regulation and cellular networks, roles in allergy and asthma, and roles in defense against infections. Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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                Author and article information

                Contributors
                zhangruiyangnjau@163.com
                zhuweiyun@njau.edu.cn
                maoshengyong@163.com
                Journal
                J Anim Sci Biotechnol
                J Anim Sci Biotechnol
                Journal of Animal Science and Biotechnology
                BioMed Central (London )
                1674-9782
                2049-1891
                29 July 2016
                29 July 2016
                2016
                : 7
                : 42
                Affiliations
                Laboratory of Gastrointestinal Microbiology, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095 Peoples Republic of China
                Article
                100
                10.1186/s40104-016-0100-1
                4966727
                27478614
                f450fae6-dcda-4206-890f-c765d91a566a
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 25 August 2015
                : 12 July 2016
                Funding
                Funded by: National Basic Research Program of the China Ministry of Science and Technology
                Award ID: 2011CB100801
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Animal science & Zoology
                dairy cows,gene expression,microarray,subacute ruminal acidosis
                Animal science & Zoology
                dairy cows, gene expression, microarray, subacute ruminal acidosis

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