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The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice
Neutrophils are thought to play an important role during contact hypersensitivity (CHS) in mice, a notion which is supported by studies in which neutrophils are depleted by monoclonal antibodies (mAb). Here, we show that administration of the commonly used anti-mouse Ly6G/C mAb (clone RB6.8C5) leads...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220669/ https://www.ncbi.nlm.nih.gov/pubmed/25400922 http://dx.doi.org/10.1002/iid3.16 |
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author | Christensen, Anne Deen Skov, Søren Haase, Claus |
author_facet | Christensen, Anne Deen Skov, Søren Haase, Claus |
author_sort | Christensen, Anne Deen |
collection | PubMed |
description | Neutrophils are thought to play an important role during contact hypersensitivity (CHS) in mice, a notion which is supported by studies in which neutrophils are depleted by monoclonal antibodies (mAb). Here, we show that administration of the commonly used anti-mouse Ly6G/C mAb (clone RB6.8C5) leads to depletion of not only neutrophils but also a population of monocytes and macrophages. In contrast, depletion using a Ly6G-specific mAb (clone 1A8) only leads to depletion of neutrophils. We demonstrate that the anti-Ly6G/C mAb suppresses the inflammatory response to a higher extent than the anti-Ly6G mAb suggesting that the impact of neutrophil-depletion in the CHS model may have been overstated when based on protocols using the anti-Ly6G/C mAb. Still, the role of neutrophils in CHS is substantiated as we demonstrate that G-CSF is an important regulator of neutrophil mobilization and effector function in CHS. Indeed, G-CSF was detectable both in the inflamed tissue and in serum during the immune response and we show that blocking G-CSF results in a reduced number of neutrophils in the blood and an attenuation of the ear-swelling response in the tissue. In conclusion, this study supports that neutrophils are important drivers of inflammation in the DNFB-induced CHS model and shows that G-CSF is a significant factor in mobilizing neutrophils during the response. |
format | Online Article Text |
id | pubmed-4220669 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-42206692014-11-06 The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice Christensen, Anne Deen Skov, Søren Haase, Claus Immun Inflamm Dis Original Research Neutrophils are thought to play an important role during contact hypersensitivity (CHS) in mice, a notion which is supported by studies in which neutrophils are depleted by monoclonal antibodies (mAb). Here, we show that administration of the commonly used anti-mouse Ly6G/C mAb (clone RB6.8C5) leads to depletion of not only neutrophils but also a population of monocytes and macrophages. In contrast, depletion using a Ly6G-specific mAb (clone 1A8) only leads to depletion of neutrophils. We demonstrate that the anti-Ly6G/C mAb suppresses the inflammatory response to a higher extent than the anti-Ly6G mAb suggesting that the impact of neutrophil-depletion in the CHS model may have been overstated when based on protocols using the anti-Ly6G/C mAb. Still, the role of neutrophils in CHS is substantiated as we demonstrate that G-CSF is an important regulator of neutrophil mobilization and effector function in CHS. Indeed, G-CSF was detectable both in the inflamed tissue and in serum during the immune response and we show that blocking G-CSF results in a reduced number of neutrophils in the blood and an attenuation of the ear-swelling response in the tissue. In conclusion, this study supports that neutrophils are important drivers of inflammation in the DNFB-induced CHS model and shows that G-CSF is a significant factor in mobilizing neutrophils during the response. Blackwell Publishing Ltd 2014-06 2014-01-03 /pmc/articles/PMC4220669/ /pubmed/25400922 http://dx.doi.org/10.1002/iid3.16 Text en © 2014 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd. http://creativecommons.org/licenses/by/3.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Christensen, Anne Deen Skov, Søren Haase, Claus The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title | The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title_full | The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title_fullStr | The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title_full_unstemmed | The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title_short | The role of neutrophils and G-CSF in DNFB-induced contact hypersensitivity in mice |
title_sort | role of neutrophils and g-csf in dnfb-induced contact hypersensitivity in mice |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220669/ https://www.ncbi.nlm.nih.gov/pubmed/25400922 http://dx.doi.org/10.1002/iid3.16 |
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