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Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model

BACKGROUND: Staphylococcus aureus causes subclinical mastitis as well as persistent and chronic infections in cattle. Bovine mastitis induced by S. aureus is often refractory to antibiotic treatment. Local innate immune defenses play an important role in eliminating the invading bacteria. TLR2 and N...

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Autores principales: Wang, Heng, Yu, Guangtao, Yu, Hui, Gu, Mingjie, Zhang, Jun, Meng, Xia, Liu, Zongping, Qiu, Changwei, Li, Jianji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672474/
https://www.ncbi.nlm.nih.gov/pubmed/25990971
http://dx.doi.org/10.1186/s13028-015-0116-0
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author Wang, Heng
Yu, Guangtao
Yu, Hui
Gu, Mingjie
Zhang, Jun
Meng, Xia
Liu, Zongping
Qiu, Changwei
Li, Jianji
author_facet Wang, Heng
Yu, Guangtao
Yu, Hui
Gu, Mingjie
Zhang, Jun
Meng, Xia
Liu, Zongping
Qiu, Changwei
Li, Jianji
author_sort Wang, Heng
collection PubMed
description BACKGROUND: Staphylococcus aureus causes subclinical mastitis as well as persistent and chronic infections in cattle. Bovine mastitis induced by S. aureus is often refractory to antibiotic treatment. Local innate immune defenses play an important role in eliminating the invading bacteria. TLR2 and NOD2 are important pathogen recognition receptors, but their functions have not been investigated in the context of early stages of mastitis. The present study examined TLR2, NOD2, and related cytokines in mammary glands infection induced by S. aureus at early stages in a rat mastitis model. FINDINGS: All inoculated mammary glands developed mastitis. Acute changes were induced in mammary tissues infected with S. aureus at early stages and then chronic infections persisted until the end of the experiment. TLR2 and NOD2 mRNA expression increased significantly after inoculation with S. aureus. The expression levels of cytokine mRNAs, including TNF-α, IL-1β, IL-6, IL-10, and CXCL1, also increased. TGF-β1 expression was suppressed at early phase and IFN-γ mRNA expression increased significantly at a later stage. CONCLUSIONS: Mammary innate immune responses were activated after S. aureus inoculation. TLR2, NOD2, and inflammatory cytokines (TNF-α, IL-1β, IL-6, CXCL1, IL-10, TGF-β1, and IFN-γ) are involved in the response to mastitis induced by S. aureus. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13028-015-0116-0) contains supplementary material, which is available to authorized users.
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spelling pubmed-46724742015-12-09 Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model Wang, Heng Yu, Guangtao Yu, Hui Gu, Mingjie Zhang, Jun Meng, Xia Liu, Zongping Qiu, Changwei Li, Jianji Acta Vet Scand Brief Communication BACKGROUND: Staphylococcus aureus causes subclinical mastitis as well as persistent and chronic infections in cattle. Bovine mastitis induced by S. aureus is often refractory to antibiotic treatment. Local innate immune defenses play an important role in eliminating the invading bacteria. TLR2 and NOD2 are important pathogen recognition receptors, but their functions have not been investigated in the context of early stages of mastitis. The present study examined TLR2, NOD2, and related cytokines in mammary glands infection induced by S. aureus at early stages in a rat mastitis model. FINDINGS: All inoculated mammary glands developed mastitis. Acute changes were induced in mammary tissues infected with S. aureus at early stages and then chronic infections persisted until the end of the experiment. TLR2 and NOD2 mRNA expression increased significantly after inoculation with S. aureus. The expression levels of cytokine mRNAs, including TNF-α, IL-1β, IL-6, IL-10, and CXCL1, also increased. TGF-β1 expression was suppressed at early phase and IFN-γ mRNA expression increased significantly at a later stage. CONCLUSIONS: Mammary innate immune responses were activated after S. aureus inoculation. TLR2, NOD2, and inflammatory cytokines (TNF-α, IL-1β, IL-6, CXCL1, IL-10, TGF-β1, and IFN-γ) are involved in the response to mastitis induced by S. aureus. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13028-015-0116-0) contains supplementary material, which is available to authorized users. BioMed Central 2015-05-20 /pmc/articles/PMC4672474/ /pubmed/25990971 http://dx.doi.org/10.1186/s13028-015-0116-0 Text en © Wang et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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.
spellingShingle Brief Communication
Wang, Heng
Yu, Guangtao
Yu, Hui
Gu, Mingjie
Zhang, Jun
Meng, Xia
Liu, Zongping
Qiu, Changwei
Li, Jianji
Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title_full Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title_fullStr Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title_full_unstemmed Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title_short Characterization of TLR2, NOD2, and related cytokines in mammary glands infected by Staphylococcus aureus in a rat model
title_sort characterization of tlr2, nod2, and related cytokines in mammary glands infected by staphylococcus aureus in a rat model
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672474/
https://www.ncbi.nlm.nih.gov/pubmed/25990971
http://dx.doi.org/10.1186/s13028-015-0116-0
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