| First Author | Wu Y | Year | 2020 |
| Journal | iScience | Volume | 23 |
| Issue | 9 | Pages | 101473 |
| PubMed ID | 32889432 | Mgi Jnum | J:308561 |
| Mgi Id | MGI:6717916 | Doi | 10.1016/j.isci.2020.101473 |
| Citation | Wu Y, et al. (2020) Selective Response to Bacterial Infection by Regulating Siglec-E Expression. iScience 23(9):101473 |
| abstractText | Interactions 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 25922 and DH5alpha) and Gram-positive bacteria (Staphylococcus aureus and Listeria monocytogenes). We found that Siglece(-/-) 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-kappaB/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. |
