دورية أكاديمية

Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing.

التفاصيل البيبلوغرافية
العنوان: Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing.
المؤلفون: Elena S Lysenko, Thomas B Clarke, Mikhail Shchepetov, Adam J Ratner, David I Roper, Christopher G Dowson, Jeffrey N Weiser
المصدر: PLoS Pathogens, Vol 3, Iss 8, p e118 (2007)
بيانات النشر: Public Library of Science (PLoS), 2007.
سنة النشر: 2007
المجموعة: LCC:Immunologic diseases. Allergy
LCC:Biology (General)
مصطلحات موضوعية: Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5
الوصف: Airway infection by the Gram-positive pathogen Streptococcus pneumoniae (Sp) leads to recruitment of neutrophils but limited bacterial killing by these cells. Co-colonization by Sp and a Gram-negative species, Haemophilus influenzae (Hi), provides sufficient stimulus to induce neutrophil and complement-mediated clearance of Sp from the mucosal surface in a murine model. Products from Hi, but not Sp, also promote killing of Sp by ex vivo neutrophil-enriched peritoneal exudate cells. Here we identify the stimulus from Hi as its peptidoglycan. Enhancement of opsonophagocytic killing was facilitated by signaling through nucleotide-binding oligomerization domain-1 (Nod1), which is involved in recognition of gamma-D-glutamyl-meso-diaminopimelic acid (meso-DAP) contained in cell walls of Hi but not Sp. Neutrophils from mice treated with Hi or compounds containing meso-DAP, including synthetic peptidoglycan fragments, showed increased Sp killing in a Nod1-dependent manner. Moreover, Nod1(-/-) mice showed reduced Hi-induced clearance of Sp during co-colonization. These observations offer insight into mechanisms of microbial competition and demonstrate the importance of Nod1 in neutrophil-mediated clearance of bacteria in vivo.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1553-7366
1553-7374
Relation: http://europepmc.org/articles/PMC1950946?pdf=render; https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374
DOI: 10.1371/journal.ppat.0030118
URL الوصول: https://doaj.org/article/25167b26826642678eeff60543a43f5d
رقم الأكسشن: edsdoj.25167b26826642678eeff60543a43f5d
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:15537366
15537374
DOI:10.1371/journal.ppat.0030118