<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Farnworth, Sarah L</style></author><author><style face="normal" font="default" size="100%">Henderson, Neil C</style></author><author><style face="normal" font="default" size="100%">Mackinnon, Alison C</style></author><author><style face="normal" font="default" size="100%">Atkinson, Kirsten M</style></author><author><style face="normal" font="default" size="100%">Wilkinson, Tom</style></author><author><style face="normal" font="default" size="100%">Dhaliwal, Kevin</style></author><author><style face="normal" font="default" size="100%">Hayashi, Katsutoshi</style></author><author><style face="normal" font="default" size="100%">Simpson, A John</style></author><author><style face="normal" font="default" size="100%">Rossi, Adriano G</style></author><author><style face="normal" font="default" size="100%">Haslett, Christopher</style></author><author><style face="normal" font="default" size="100%">Sethi, Tariq</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Galectin-3 reduces the severity of pneumococcal pneumonia by augmenting neutrophil function.</style></title><secondary-title><style face="normal" font="default" size="100%">The American journal of pathology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Pathol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Flow Cytometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Galectin 3</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Macrophages</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Mutant Strains</style></keyword><keyword><style  face="normal" font="default" size="100%">Neutrophil Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Neutrophils</style></keyword><keyword><style  face="normal" font="default" size="100%">Phagocytosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Pneumonia, Pneumococcal</style></keyword><keyword><style  face="normal" font="default" size="100%">Streptococcus pneumoniae</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">172</style></volume><pages><style face="normal" font="default" size="100%">395-405</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The Gram-positive Streptococcus pneumoniae is the leading cause of community-acquired pneumonia worldwide, resulting in high mortality. Our in vivo studies show that galectin-3(-/-) mice develop more severe pneumonia after infection with S. pneumoniae, as demonstrated by increased bacteremia and lung damage compared to wild-type mice and that galectin-3 reduces the severity of pneumococcal pneumonia in part by augmenting neutrophil function. Specifically, we show that 1) galectin-3 directly acts as a neutrophil-activating agent and potentiates the effect of fMLP, 2) exogenous galectin-3 augments neutrophil phagocytosis of bacteria and delays neutrophil apoptosis, 3) phagocytosis of apoptotic neutrophils by galectin-3(-/-) macrophages is less efficient compared to wild type, and 4) galectin-3 demonstrates bacteriostatic properties against S. pneumoniae in vitro. Furthermore, ad-back of recombinant galectin-3 in vivo protects galectin-3-deficient mice from developing severe pneumonia. Together, these results demonstrate that galectin-3 is a key molecule in the host defense against pneumococcal infection. Therapeutic strategies designed to augment galectin-3 activity may both enhance inflammatory cell function (by directly affecting neutrophil responsiveness and prolonging neutrophil longevity) and have direct bacteriostatic activity, improving clinical outcomes after severe pneumococcal infection.</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18202191?dopt=Abstract</style></custom1></record></records></xml>