References
Query Results -- Details
MGI Accession ID: MGI:3773603
J Number: J:131407
Other Accession IDs:
Title: Galectin-3 reduces the severity of pneumococcal pneumonia by augmenting neutrophil function.
Authors: Farnworth SL; Henderson NC; Mackinnon AC; Atkinson KM; Wilkinson T; Dhaliwal K; Hayashi K; Simpson AJ; Rossi AG; Haslett C; Sethi T
Journal: Am J Pathol
Volume: 172
Issue: 2
Date: 2008 Feb
Year: 2008
Pages: 395-405
Review Status: Peer Reviewed
Abstract:
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.
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