Selective Response to Bacterial Infection by Regulating Siglec-E Expression
Summary: 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 nonsialylate...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2020-09-01
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| Series: | iScience |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004220306659 |
| _version_ | 1818545258510680064 |
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| author | Yin Wu Darong Yang Runhua Liu Lizhong Wang Guo-Yun Chen |
| author_facet | Yin Wu Darong Yang Runhua Liu Lizhong Wang Guo-Yun Chen |
| author_sort | Yin Wu |
| collection | DOAJ |
| description | Summary: 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 DH5α) 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-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. |
| first_indexed | 2024-12-12T02:59:05Z |
| format | Article |
| id | doaj.art-6b2087ef1f084c99a9f47ddc4400788f |
| institution | Directory Open Access Journal |
| issn | 2589-0042 |
| language | English |
| last_indexed | 2024-12-12T02:59:05Z |
| publishDate | 2020-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | iScience |
| spelling | doaj.art-6b2087ef1f084c99a9f47ddc4400788f2022-12-22T00:40:40ZengElsevieriScience2589-00422020-09-01239101473Selective Response to Bacterial Infection by Regulating Siglec-E ExpressionYin Wu0Darong Yang1Runhua Liu2Lizhong Wang3Guo-Yun Chen4Children's Foundation Research Institute at Le Bonheur Children's Hospital, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USAChildren's Foundation Research Institute at Le Bonheur Children's Hospital, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USADepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USADepartment of Genetics, University of Alabama at Birmingham, Birmingham, AL, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, USAChildren's Foundation Research Institute at Le Bonheur Children's Hospital, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN 38103, USA; Corresponding authorSummary: 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 DH5α) 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-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.http://www.sciencedirect.com/science/article/pii/S2589004220306659GeneticsMolecular BiologyMicrobiology |
| spellingShingle | Yin Wu Darong Yang Runhua Liu Lizhong Wang Guo-Yun Chen Selective Response to Bacterial Infection by Regulating Siglec-E Expression iScience Genetics Molecular Biology Microbiology |
| title | Selective Response to Bacterial Infection by Regulating Siglec-E Expression |
| title_full | Selective Response to Bacterial Infection by Regulating Siglec-E Expression |
| title_fullStr | Selective Response to Bacterial Infection by Regulating Siglec-E Expression |
| title_full_unstemmed | Selective Response to Bacterial Infection by Regulating Siglec-E Expression |
| title_short | Selective Response to Bacterial Infection by Regulating Siglec-E Expression |
| title_sort | selective response to bacterial infection by regulating siglec e expression |
| topic | Genetics Molecular Biology Microbiology |
| url | http://www.sciencedirect.com/science/article/pii/S2589004220306659 |
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