摘要：SummaryInteractions between microbes and hosts can be a benign, deleterious, or even fatal, resulting in death of the host, the microbe, or both. Sialic acid-binding immunoglobulin-like lectins (Siglecs) suppress infection responses to sialylated pathogens. However, most pathogens are nonsialylated. Here we determined Siglecs respond to nonsialylated Gram-negative bacteria (Escherichia coli 25922andDH5α) and Gram-positive bacteria (Staphylococcus aureusandListeria monocytogenes). We found thatSiglece−/−mice had higher mortality than wild-type mice following Gram-negative but not Gram-positive bacterial infection. Better survival in wild-type mice depended on more efficient clearance of Gram-negative than Gram-positive bacteria. Gram-negative bacteria upregulated Siglec-E, thus increasing reactive oxygen species (ROS); Tyr432 in the ITIM domain of Siglec-E was required to increase ROS. Moreover, Gram-negative bacteria upregulated Siglec-E via TLR4/MyD88/JNK/NF-κB/AP-1, whereas Gram-positive bacteria downregulated Siglec-E via TLR2/RANKL/TRAF6/Syk. Thus, our study describes a fundamentally new role for Siglec-E during infection.Graphical AbstractDisplay OmittedHighlights•Siglec-E controls bacterial survival by regulating ROS generation•Gram-negative bacteria upregulated Siglec-E via TLR4/MyD88/JNK/NF-κB/AP-1•Gram-positive bacteria downregulated Siglec-E via TLR2/RANKL/TRAF6/SykGenetics; Molecular Biology; Microbiology
