Imperial College London


Faculty of MedicineDepartment of Medicine

Research Fellow



+44 (0)20 7594 2074thomas.clarke




5.40CFlowers buildingSouth Kensington Campus






BibTex format

author = {Lysenko, ES and Clarke, TB and Shchepetov, M and Ratner, AJ and Roper, DI and Dowson, CG and Weiser, JN},
doi = {10.1371/journal.ppat.0030118},
journal = {PLoS Pathog},
title = {Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing.},
url = {},
volume = {3},
year = {2007}

RIS format (EndNote, RefMan)

AB - 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.
AU - Lysenko,ES
AU - Clarke,TB
AU - Shchepetov,M
AU - Ratner,AJ
AU - Roper,DI
AU - Dowson,CG
AU - Weiser,JN
DO - 10.1371/journal.ppat.0030118
PY - 2007///
TI - Nod1 signaling overcomes resistance of S. pneumoniae to opsonophagocytic killing.
T2 - PLoS Pathog
UR -
UR -
VL - 3
ER -