Abstract
The innate immune system employs C-type lectin receptors (CLRs) to recognize carbohydrate structures on pathogens and self-antigens. The Macrophage-inducible C-type lectin (Mincle) is a FcRγ-coupled CLR that was shown to bind to mycobacterial cord factor as well as certain fungal species. However, since CLR functions during bacterial infections have not yet been investigated thoroughly, we aimed to examine their function in Streptococcus pneumonia infection. Binding studies using a library of recombinantly expressed CLR-Fc fusion proteins indicated a specific, Ca2+-dependent, and serotype-specific binding of Mincle to S. pneumonia. Subsequent experiments with different Mincle-expressing cells as well as Mincle-deficient mice, however, revealed a limited role of this receptor in bacterial phagocytosis, neutrophil-mediated killing, cytokine production, and antibacterial immune response during pneumonia. Collectively, our results indicate that Mincle is able to recognize S. pneumonia but is not required for the anti-pneumococcal innate immune response.
Highlights
Streptococcus pneumoniae frequently colonizes the upper respiratory tract of humans
To analyze whether C-type lectin receptors (CLRs) are involved in S. pneumoniae recognition, we performed an initial ELISA screening for CLR binding to heat-killed S. pneumoniae ST3 using a comprehensive library of CLR-Fc fusion proteins [37] (Fig. 1A)
These findings indicate that Macrophage-inducible C-type lectin (Mincle) recognizes S. pneumoniae
Summary
Streptococcus pneumoniae frequently colonizes the upper respiratory tract of humans. Depending on the immune status of the host, on preceding viral infections, and on the pneumococcal serotype, this asymptomatic colonization can progress to invasive diseases. These diseases, that include community-acquired pneumonia, sepsis, and meningitis, cause significant mortality especially in children and the elderly [1, 2]. Important virulence factors of S. pneumoniae are PLOS ONE | DOI:10.1371/journal.pone.0117022. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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