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The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence
Mastitis, inflammation of the mammary gland, is a common disease of dairy animals. The disease is caused by bacterial infection ascending through the teat canal and mammary pathogenic Escherichia coli (MPEC) are common etiology. In the first phase of infection, virulence mechanisms, designated as ni...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294653/ https://www.ncbi.nlm.nih.gov/pubmed/32539761 http://dx.doi.org/10.1186/s13567-020-00804-x |
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author | Salamon, Hagit Nissim-Eliraz, Einat Ardronai, Oded Nissan, Israel Shpigel, Nahum Y. |
author_facet | Salamon, Hagit Nissim-Eliraz, Einat Ardronai, Oded Nissan, Israel Shpigel, Nahum Y. |
author_sort | Salamon, Hagit |
collection | PubMed |
description | Mastitis, inflammation of the mammary gland, is a common disease of dairy animals. The disease is caused by bacterial infection ascending through the teat canal and mammary pathogenic Escherichia coli (MPEC) are common etiology. In the first phase of infection, virulence mechanisms, designated as niche factors, enable MPEC bacteria to resist innate antimicrobial mechanisms, replicate in milk, and to colonize the mammary gland. Next, massive replication of colonizing bacteria culminates in a large biomass of microbe-associated molecular patterns (MAMPs) recognized by pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) mediating inflammatory signaling in mammary alveolar epithelial cells (MAEs) and macrophages. Bacterial lipopolysaccharides (LPSs), the prototypical class of MAMPs are sufficient to elicit mammary inflammation mediated by TLR4 signaling and activation of nuclear factor kB (NF-kB), the master regulator of inflammation. Using in vivo mastitis model, in low and high complements mice, and in vitro NF-kB luminescence reporter system in MAEs, we have found that the smooth configuration of LPS O-polysaccharides in MPEC enables the colonizing organisms to evade the host immune response by reducing inflammatory response and conferring resistance to complement. Screening a collection of MPEC field strains, we also found that all strains were complement resistant and 94% (45/48) were smooth. These results indicate that the structure of LPS O-polysaccharides chain is important for the pathogenesis of MPEC mastitis and provides protection against complement-mediated killing. Furthermore, we demonstrate a role for complement, a key component of innate immunity, in host-microbe interactions of the mammary gland. |
format | Online Article Text |
id | pubmed-7294653 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-72946532020-06-16 The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence Salamon, Hagit Nissim-Eliraz, Einat Ardronai, Oded Nissan, Israel Shpigel, Nahum Y. Vet Res Research Article Mastitis, inflammation of the mammary gland, is a common disease of dairy animals. The disease is caused by bacterial infection ascending through the teat canal and mammary pathogenic Escherichia coli (MPEC) are common etiology. In the first phase of infection, virulence mechanisms, designated as niche factors, enable MPEC bacteria to resist innate antimicrobial mechanisms, replicate in milk, and to colonize the mammary gland. Next, massive replication of colonizing bacteria culminates in a large biomass of microbe-associated molecular patterns (MAMPs) recognized by pattern recognition receptors (PRRs) such as toll-like receptors (TLRs) mediating inflammatory signaling in mammary alveolar epithelial cells (MAEs) and macrophages. Bacterial lipopolysaccharides (LPSs), the prototypical class of MAMPs are sufficient to elicit mammary inflammation mediated by TLR4 signaling and activation of nuclear factor kB (NF-kB), the master regulator of inflammation. Using in vivo mastitis model, in low and high complements mice, and in vitro NF-kB luminescence reporter system in MAEs, we have found that the smooth configuration of LPS O-polysaccharides in MPEC enables the colonizing organisms to evade the host immune response by reducing inflammatory response and conferring resistance to complement. Screening a collection of MPEC field strains, we also found that all strains were complement resistant and 94% (45/48) were smooth. These results indicate that the structure of LPS O-polysaccharides chain is important for the pathogenesis of MPEC mastitis and provides protection against complement-mediated killing. Furthermore, we demonstrate a role for complement, a key component of innate immunity, in host-microbe interactions of the mammary gland. BioMed Central 2020-06-15 2020 /pmc/articles/PMC7294653/ /pubmed/32539761 http://dx.doi.org/10.1186/s13567-020-00804-x Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data. |
spellingShingle | Research Article Salamon, Hagit Nissim-Eliraz, Einat Ardronai, Oded Nissan, Israel Shpigel, Nahum Y. The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title | The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title_full | The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title_fullStr | The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title_full_unstemmed | The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title_short | The role of O-polysaccharide chain and complement resistance of Escherichia coli in mammary virulence |
title_sort | role of o-polysaccharide chain and complement resistance of escherichia coli in mammary virulence |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294653/ https://www.ncbi.nlm.nih.gov/pubmed/32539761 http://dx.doi.org/10.1186/s13567-020-00804-x |
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