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*
Glycobiology Laboratory,
Research Center for Infectious Disease, Laval University Medical Center, Centre Hospitalier Universitaire de Québec, Québec, Canada
Recruitment of neutrophils from blood vessels to sites of infection
represents one of the most important elements of innate immunity.
Movement of neutrophils across blood vessel walls to the site of
infection first requires that the migrating cells firmly attach to the
endothelial wall. Generally, neutrophil extravasation is mediated at
least in part by two classes of adhesion molecules, 
2
integrins and selectins. However, in the case of streptococcal
pneumonia, recent studies have revealed that a significant proportion
of neutrophil diapedesis is not mediated by the 2
integrin/selectin paradigm. Galectin-3 is a -galactoside-binding
lectin implicated in inflammatory responses as well as in cell
adhesion. Using an in vivo streptococcal pneumonia mouse model, we
found that accumulation of galectin-3 in the alveolar space of
streptococcus-infected lungs correlates closely with the onset of
neutrophil extravasation. Furthermore, immunohistological analysis of
infected lung tissue revealed the presence of galectin-3 in the lung
tissue areas composed of epithelial and endothelial cell layers as well
as of interstitial spaces. In vitro, galectin-3 was able to promote
neutrophil adhesion to endothelial cells. Promotion of neutrophil
adhesion by galectin-3 appeared to result from direct cross-linking of
neutrophils to the endothelium and was dependent on galectin-3
oligomerization. Together, these results suggest that galectin-3 acts
as an adhesion molecule that can mediate neutrophil adhesion to
endothelial cells. However, accumulation of galectin-3 in lung was not
observed during neutrophil emigration into alveoli induced by
Escherichia coli infection, where the majority of
neutrophil emigration is known to be 2 integrin
dependent. Thus, based on our results, we propose that galectin-3 plays
a role in 2 integrin-independent neutrophil
extravasation, which occurs during alveolar infection with
Streptococcus
pneumoniae.
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