Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing
Lysenko, Elena S., Clarke, Thomas B., Shchepetov, Mikhail, Ratner, Adam J., Roper, David I., Dowson, Christopher G. and Weiser, Jeffrey N.. (2007) Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing. PLoS Pathogens, Vol.3 (No.8). pp. 1073-1081. ISSN 1553-7374Full text not available from this repository.
Official URL: http://dx.doi.org/10.1371/journal.ppat.0030118
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.
|Item Type:||Journal Article|
|Subjects:||Q Science > QR Microbiology > QR355 Virology
Q Science > QR Microbiology
Q Science > QL Zoology
|Divisions:||Faculty of Science > Life Sciences (2010- ) > Biological Sciences ( -2010)|
|Journal or Publication Title:||PLoS Pathogens|
|Publisher:||Public Library of Science|
|Number of Pages:||9|
|Page Range:||pp. 1073-1081|
|Access rights to Published version:||Open Access|
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