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Role of Galectin-3 in Leukocyte Recruitment in a Murine Model of Lung Infection by Streptococcus pneumoniae¹

Julie Nieminen^*, Christian St-Pierre^*, Pampa Bhaumik^*, Françoise Poirier and Sachiko Sato^2,*

^* Glycobiology Laboratory, Research Center for Infectious Diseases, Faculty of Medicine, Laval University, Québec, Canada; and Laboratoire de Genetique et Developpement des Mammiferes, Institut Jacques Monod, UMR CNRS 7592, Universités Paris 6 and Paris 7, Paris, France

Pneumonia can be caused by a variety of pathogens, among which Streptococcus pneumoniae causes one of the most common forms of community-acquired pneumonia. Depending on the invading pathogen, the elements of the immune response triggered will vary. For most pathogens, such as Escherichia coli, neutrophil recruitment involves a well-described family of adhesion molecules, β₂-integrins. In the case of streptococcal pneumonia, however, neutrophil recruitment occurs mainly through a β₂-integrin-independent pathway. Despite decades of research on this issue, the adhesion molecules involved in neutrophil recruitment during lung infection by S. pneumoniae have not been identified. We have previously shown that galectin-3, a soluble mammalian lectin, can be found in lungs infected by S. pneumoniae, but not by E. coli, and can mediate the adhesion of neutrophils on the endothelial cell layer, implying its role in the recruitment of neutrophils to lungs infected with S. pneumoniae. In this study, using galectin-3 null mice, we report further evidence of the involvement of this soluble lectin in the recruitment of neutrophils to S. pneumonia-infected lungs. Indeed, in the absence of galectin-3, lower numbers of leukocytes, mainly neutrophils, were recruited to the infected lungs during infection by S. pneumoniae. In the case of β₂-integrin-dependent recruitment induced by lung infection with E. coli, the number of recruited neutrophils was not reduced. Thus, taken together, our data suggest that galectin-3 plays a role as a soluble adhesion molecule in the recruitment of neutrophils to lungs infected by S. pneumoniae, which induces β₂-integrin-independent migration.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Canadian Institutes of Health Research, the Mizutani Foundation for Glycoscience, and by equipment grants from the Canadian Foundation for Innovation (to S.S.). S.S. is a senior scholar of the Fonds de la Recherche en Santé du Québec.

² Address correspondence and reprint requests to Dr. Sachiko Sato, Glycobiology Laboratory, Centre de Recherche en Infectiologie, Centre Hospitalier de l’Université Laval, 2705 boul. Laurier, Ste-Foy, Québec, Canada, G1V 4G2. E-mail address: Sachiko.Sato{at}crchul.ulaval.ca

³ Abbreviations used in this paper: WT, wild type; BAL, bronchoalveolar lavage; KO, knock out; MPO, myeloperoxidase; KC, keratinocyte chemoattractant.

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