دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice.
المؤلفون: 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
المصدر: PLoS Pathogens, Vol 8, Iss 11, p e1003047 (2012)
بيانات النشر: Public Library of Science (PLoS), 2012.
سنة النشر: 2012
المجموعة: LCC:Immunologic diseases. Allergy
LCC:Biology (General)
مصطلحات موضوعية: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
الوصف: 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1553-7366
1553-7374
Relation: https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23209417/?tool=EBI; https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374
DOI: 10.1371/journal.ppat.1003047
URL الوصول: https://doaj.org/article/537606f4a0f84c01b78748202198eeae
رقم الأكسشن: edsdoj.537606f4a0f84c01b78748202198eeae
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:15537366
15537374
DOI:10.1371/journal.ppat.1003047