Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.

Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis and in vivo multispectral noninvasive imaging during the...

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Autores principales: John S Cho, Yi Guo, Romela Irene Ramos, Frank Hebroni, Seema B Plaisier, Caiyun Xuan, Jennifer L Granick, Hironori Matsushima, Akira Takashima, Yoichiro Iwakura, Ambrose L Cheung, Genhong Cheng, Delphine J Lee, Scott I Simon, Lloyd S Miller
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:537606f4a0f84c01b78748202198eeae2021-11-18T06:06:18ZNeutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.1553-73661553-737410.1371/journal.ppat.1003047https://doaj.org/article/537606f4a0f84c01b78748202198eeae2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23209417/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis and in vivo multispectral noninvasive imaging during the S. aureus infection revealed a strong functional and temporal association between neutrophil recruitment and IL-1β/IL-1R activation. Unexpectedly, neutrophils but not monocytes/macrophages or other MHCII-expressing antigen presenting cells were the predominant source of IL-1β at the site of infection. Furthermore, neutrophil-derived IL-1β was essential for host defense since adoptive transfer of IL-1β-expressing neutrophils was sufficient to restore the impaired neutrophil abscess formation in S. aureus-infected IL-1β-deficient mice. S. aureus-induced IL-1β production by neutrophils required TLR2, NOD2, FPR1 and the ASC/NLRP3 inflammasome in an α-toxin-dependent mechanism. Taken together, IL-1β and neutrophil abscess formation during an infection are functionally, temporally and spatially linked as a consequence of direct IL-1β production by neutrophils.John S ChoYi GuoRomela Irene RamosFrank HebroniSeema B PlaisierCaiyun XuanJennifer L GranickHironori MatsushimaAkira TakashimaYoichiro IwakuraAmbrose L CheungGenhong ChengDelphine J LeeScott I SimonLloyd S MillerPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 8, Iss 11, p e1003047 (2012)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
John S Cho
Yi Guo
Romela Irene Ramos
Frank Hebroni
Seema B Plaisier
Caiyun Xuan
Jennifer L Granick
Hironori Matsushima
Akira Takashima
Yoichiro Iwakura
Ambrose L Cheung
Genhong Cheng
Delphine J Lee
Scott I Simon
Lloyd S Miller
Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
description Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis and in vivo multispectral noninvasive imaging during the S. aureus infection revealed a strong functional and temporal association between neutrophil recruitment and IL-1β/IL-1R activation. Unexpectedly, neutrophils but not monocytes/macrophages or other MHCII-expressing antigen presenting cells were the predominant source of IL-1β at the site of infection. Furthermore, neutrophil-derived IL-1β was essential for host defense since adoptive transfer of IL-1β-expressing neutrophils was sufficient to restore the impaired neutrophil abscess formation in S. aureus-infected IL-1β-deficient mice. S. aureus-induced IL-1β production by neutrophils required TLR2, NOD2, FPR1 and the ASC/NLRP3 inflammasome in an α-toxin-dependent mechanism. Taken together, IL-1β and neutrophil abscess formation during an infection are functionally, temporally and spatially linked as a consequence of direct IL-1β production by neutrophils.
format article
author John S Cho
Yi Guo
Romela Irene Ramos
Frank Hebroni
Seema B Plaisier
Caiyun Xuan
Jennifer L Granick
Hironori Matsushima
Akira Takashima
Yoichiro Iwakura
Ambrose L Cheung
Genhong Cheng
Delphine J Lee
Scott I Simon
Lloyd S Miller
author_facet John S Cho
Yi Guo
Romela Irene Ramos
Frank Hebroni
Seema B Plaisier
Caiyun Xuan
Jennifer L Granick
Hironori Matsushima
Akira Takashima
Yoichiro Iwakura
Ambrose L Cheung
Genhong Cheng
Delphine J Lee
Scott I Simon
Lloyd S Miller
author_sort John S Cho
title Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
title_short Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
title_full Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
title_fullStr Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
title_full_unstemmed Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
title_sort neutrophil-derived il-1β is sufficient for abscess formation in immunity against staphylococcus aureus in mice.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/537606f4a0f84c01b78748202198eeae
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