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ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages
Avian leucosis virus subgroup J (ALV-J) can cause lifelong infection and can escape from the host immune defenses in chickens. Since macrophages act as the important defense line against invading pathogens in host innate immunity, we investigated the function and innate immune responses of chicken p...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Poultry Science Association, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161024/ https://www.ncbi.nlm.nih.gov/pubmed/27486255 http://dx.doi.org/10.3382/ps/pew229 |
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author | Feng, Min Dai, Manman Cao, Weisheng Tan, Yan Li, Zhenhui Shi, Meiqing Zhang, Xiquan |
author_facet | Feng, Min Dai, Manman Cao, Weisheng Tan, Yan Li, Zhenhui Shi, Meiqing Zhang, Xiquan |
author_sort | Feng, Min |
collection | PubMed |
description | Avian leucosis virus subgroup J (ALV-J) can cause lifelong infection and can escape from the host immune defenses in chickens. Since macrophages act as the important defense line against invading pathogens in host innate immunity, we investigated the function and innate immune responses of chicken primary monocyte-derived macrophages (MDM) after ALV-J infection in this study. Our results indicated that ALV-J was stably maintained in MDM cells but that the viral growth rate was significantly lower than that in DF-1 cells. We also found that ALV-J infection significantly increased nitric oxide (NO) production, but had no effect on MDM phagocytic capacity. Interestingly, infection with ALV-J rapidly promoted the expression levels of Myxovirus resistance 1 (Mx) (3 h, 6 h), ISG12 (6 h), and interleukin-1β (IL-1β) (3 h, 12 h) at an early infection stage, whereas it sharply decreased the expression of Mx (24 h, 36 h), ISG12 (36 h), and made little change on IL-1β (24 h, 36 h) production at a late infection stage in MDM cells. Moreover, the protein levels of interferon-β (IFN-β) and interleukin-6 (IL-6) had sharply increased in infected MDM cells from 3 to 36 h post infection (hpi) of ALV-J. And, the protein level of interleukin-10 (IL-10) was dramatically decreased at 36 hpi in MDM cells infected with ALV-J. These results demonstrate that ALV-J can induce host innate immune responses and we hypothesize that macrophages play an important role in host innate immune attack and ALV-J immune escape. |
format | Online Article Text |
id | pubmed-5161024 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Poultry Science Association, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-51610242016-12-19 ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages Feng, Min Dai, Manman Cao, Weisheng Tan, Yan Li, Zhenhui Shi, Meiqing Zhang, Xiquan Poult Sci Immunology, Health and Disease Avian leucosis virus subgroup J (ALV-J) can cause lifelong infection and can escape from the host immune defenses in chickens. Since macrophages act as the important defense line against invading pathogens in host innate immunity, we investigated the function and innate immune responses of chicken primary monocyte-derived macrophages (MDM) after ALV-J infection in this study. Our results indicated that ALV-J was stably maintained in MDM cells but that the viral growth rate was significantly lower than that in DF-1 cells. We also found that ALV-J infection significantly increased nitric oxide (NO) production, but had no effect on MDM phagocytic capacity. Interestingly, infection with ALV-J rapidly promoted the expression levels of Myxovirus resistance 1 (Mx) (3 h, 6 h), ISG12 (6 h), and interleukin-1β (IL-1β) (3 h, 12 h) at an early infection stage, whereas it sharply decreased the expression of Mx (24 h, 36 h), ISG12 (36 h), and made little change on IL-1β (24 h, 36 h) production at a late infection stage in MDM cells. Moreover, the protein levels of interferon-β (IFN-β) and interleukin-6 (IL-6) had sharply increased in infected MDM cells from 3 to 36 h post infection (hpi) of ALV-J. And, the protein level of interleukin-10 (IL-10) was dramatically decreased at 36 hpi in MDM cells infected with ALV-J. These results demonstrate that ALV-J can induce host innate immune responses and we hypothesize that macrophages play an important role in host innate immune attack and ALV-J immune escape. Poultry Science Association, Inc. 2016-08-02 2017-01 /pmc/articles/PMC5161024/ /pubmed/27486255 http://dx.doi.org/10.3382/ps/pew229 Text en © The Author 2016. Published by Oxford University Press on behalf of Poultry Science Association. http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Immunology, Health and Disease Feng, Min Dai, Manman Cao, Weisheng Tan, Yan Li, Zhenhui Shi, Meiqing Zhang, Xiquan ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title | ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title_full | ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title_fullStr | ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title_full_unstemmed | ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title_short | ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages |
title_sort | alv-j strain scau-hn06 induces innate immune responses in chicken primary monocyte-derived macrophages |
topic | Immunology, Health and Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161024/ https://www.ncbi.nlm.nih.gov/pubmed/27486255 http://dx.doi.org/10.3382/ps/pew229 |
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