PSGL-1 on leukocytes is a critical component of the host immune response against invasive pneumococcal disease
Entity
UAM. Departamento de Medicina; Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)Publisher
Public Library of ScienceDate
2016-03-01Citation
10.1371/journal.ppat.1005500
PloS Pathogens 12.3 (2016): e1005500
ISSN
1553-7366DOI
10.1371/journal.ppat.1005500Funded by
This work was supported by grants SAF2012-39444-C01/02 from Ministerio de Economía y Competitividad (MINECO) to EG and JYProject
Gobierno de España. SAF2012-39444-C01/02Editor's Version
http://dx.doi.org/10.1371/journal.ppat.1005500Subjects
Streptococcus pneumoniae; PSGL-1; Leukocytes; Pneumococcal disease; MedicinaRights
© 2016 Ramos-Sevillano et alAbstract
Bacterial uptake by phagocytic cells is a vital event in the clearance of invading pathogens such as Streptococcus pneumoniae. A major role of the P-selectin glycoprotein ligand-1 (PSGL-1) on leukocytes against invasive pneumococcal disease is described in this study. Phagocytosis experiments using different serotypes demonstrated that PSGL-1 is involved in the recognition, uptake and killing of S. pneumoniae. Co-localization of several clinical isolates of S. pneumoniae with PSGL-1 was demonstrated, observing a rapid and active phagocytosis in the presence of PSGL-1. Furthermore, the pneumococcal capsular polysaccharide and the main autolysin of the bacterium ―the amidase LytA― were identified as bacterial ligands for PSGL-1. Experimental models of pneumococcal disease including invasive pneumonia and systemic infection showed that bacterial levels were markedly increased in the blood of PSGL-1−/− mice. During pneumonia, PSGL-1 controls the severity of pneumococcal dissemination from the lung to the bloodstream. In systemic infection, a major role of PSGL-1 in host defense is to clear the bacteria in the systemic circulation controlling bacterial replication. These results confirmed the importance of this receptor in the recognition and clearance of S. pneumoniae during invasive pneumococcal disease. Histological and cellular analysis demonstrated that PSGL-1−/− mice have increased levels of T cells migrating to the lung than the corresponding wild-type mice. In contrast, during systemic infection, PSGL-1−/− mice had increased numbers of neutrophils and macrophages in blood, but were less effective controlling the infection process due to the lack of this functional receptor. Overall, this study demonstrates that PSGL-1 is a novel receptor for S. pneumoniae that contributes to protection against invasive pneumococcal disease.
Files in this item
Google Scholar:Ramos-Sevillano, Elisa
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Urzainqui, Ana
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Andrés, Belén de
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González-Tajuelo, Rafael
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Domenech, Mirian
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González-Camacho, Fernando
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Sánchez Madrid, Francisco
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Brown, Jeremy S.
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García, Ernesto
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Yuste, José
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