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Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin
The skin functions as a protective barrier to inhibit the entry of foreign pathogens, all the while hosting a diverse milieu of microorganisms. Over time, skin cells, immune cells, cytokines, and microbes interact to integrate the processes of maintaining the skin’s physical and immune barrier. In t...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8290525/ https://www.ncbi.nlm.nih.gov/pubmed/34295313 http://dx.doi.org/10.3389/fmicb.2021.658980 |
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author | Luckett-Chastain, Lerin R. King, Catherine J. McShan, William M. Gipson, Jenny R. Gillaspy, Allison F. Gallucci, Randle M. |
author_facet | Luckett-Chastain, Lerin R. King, Catherine J. McShan, William M. Gipson, Jenny R. Gillaspy, Allison F. Gallucci, Randle M. |
author_sort | Luckett-Chastain, Lerin R. |
collection | PubMed |
description | The skin functions as a protective barrier to inhibit the entry of foreign pathogens, all the while hosting a diverse milieu of microorganisms. Over time, skin cells, immune cells, cytokines, and microbes interact to integrate the processes of maintaining the skin’s physical and immune barrier. In the present study, the basal expression of two immunologically divergent mouse strains C57BL/6 and BALB/c, as well as a strain on the C57 background lacking IL-6, was characterized. Additionally, cutaneous antimicrobial gene expression profiles and skin bacterial microbiome were assessed between strains. Total RNA sequencing was performed on untreated C57BL/6 (control), BALB/c, and IL-6-deficient skin samples and found over 3,400 genes differentially modulated between strains. It was found that each strain modulated its own transcriptional “profile” associated with skin homeostasis and also influenced the overall bacterial colonization as indicated by the differential phyla present on each strain. Together, these data not only provide a comprehensive view of the transcriptional changes in homeostatic skin of different mouse strains but also highlight the possible influence of the strain differences (e.g., Th1/Th2 balance) as well as a role for IL-6 in overall skin immunity and resident microbial populations. |
format | Online Article Text |
id | pubmed-8290525 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82905252021-07-21 Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin Luckett-Chastain, Lerin R. King, Catherine J. McShan, William M. Gipson, Jenny R. Gillaspy, Allison F. Gallucci, Randle M. Front Microbiol Microbiology The skin functions as a protective barrier to inhibit the entry of foreign pathogens, all the while hosting a diverse milieu of microorganisms. Over time, skin cells, immune cells, cytokines, and microbes interact to integrate the processes of maintaining the skin’s physical and immune barrier. In the present study, the basal expression of two immunologically divergent mouse strains C57BL/6 and BALB/c, as well as a strain on the C57 background lacking IL-6, was characterized. Additionally, cutaneous antimicrobial gene expression profiles and skin bacterial microbiome were assessed between strains. Total RNA sequencing was performed on untreated C57BL/6 (control), BALB/c, and IL-6-deficient skin samples and found over 3,400 genes differentially modulated between strains. It was found that each strain modulated its own transcriptional “profile” associated with skin homeostasis and also influenced the overall bacterial colonization as indicated by the differential phyla present on each strain. Together, these data not only provide a comprehensive view of the transcriptional changes in homeostatic skin of different mouse strains but also highlight the possible influence of the strain differences (e.g., Th1/Th2 balance) as well as a role for IL-6 in overall skin immunity and resident microbial populations. Frontiers Media S.A. 2021-07-06 /pmc/articles/PMC8290525/ /pubmed/34295313 http://dx.doi.org/10.3389/fmicb.2021.658980 Text en Copyright © 2021 Luckett-Chastain, King, McShan, Gipson, Gillaspy and Gallucci. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Luckett-Chastain, Lerin R. King, Catherine J. McShan, William M. Gipson, Jenny R. Gillaspy, Allison F. Gallucci, Randle M. Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title | Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title_full | Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title_fullStr | Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title_full_unstemmed | Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title_short | Loss of Interleukin-6 Influences Transcriptional Immune Signatures and Alters Bacterial Colonization in the Skin |
title_sort | loss of interleukin-6 influences transcriptional immune signatures and alters bacterial colonization in the skin |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8290525/ https://www.ncbi.nlm.nih.gov/pubmed/34295313 http://dx.doi.org/10.3389/fmicb.2021.658980 |
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