Pathobiont-driven antibody sialylation through IL-10 undermines vaccination
The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protect...
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| Published in | The Journal of clinical investigation Vol. 134; no. 24 |
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| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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American Society for Clinical Investigation
16.12.2024
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| Abstract | The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy. |
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| AbstractList | The pathobiont
Staphylococcus aureus
(Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall–associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti–
Streptococcus pyogenes
and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy.
There hasn’t been a successful staphylococcal vaccine to date. We show that S. aureus induces IL-10 which abrogates protective anti-staphylococcal antibody function through hyper-sialylation. The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy. The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy.The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy. The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-[alpha]2,3sialylation of antibodies and loss of protective activity. IL-10 enhances [alpha]2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy. |
| Audience | Academic |
| Author | Liu, George Y. Hajam, Irshad A. Tsai, Chih-Ming Lin, Brian Lewis, Nathan E. Choudhruy, Biswa Wierzbicki, Igor H. Chiang, Austin W.T. Askarian, Fatemeh Caldera, J.R. Du Gonzalez, David J. Suzuki, Emi Clark, Ty’Tianna Conrad, Douglas J. Riestra, Angelica M. Gonzalez, Cesia Li, Haining Nizet, Victor |
| AuthorAffiliation | 5 Division of Gastroenterology, Department of Pediatrics, UCSD, La Jolla, California, USA 10 Division of Pulmonary, Critical Care and Sleep Medicine, UCSD, La Jolla, California, USA 4 Department of Bioengineering, University of California, La Jolla, California, USA 3 Glycobiology Research and Training Center, UCSD, La Jolla, California, USA 8 Department of Biology, San Diego State University, San Diego, California, USA 1 Division of Infectious Diseases, Department of Pediatrics, University of California, La Jolla, California, USA 6 Division of Gastroenterology, Rady Children’s Hospital, San Diego, California, USA 7 Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, UC San Diego School of Medicine, La Jolla, California, USA 9 Skaggs School of Pharmacy and Pharmaceutical Sciences, UCSD, La Jolla, California, USA 2 Immunology Center of Georgia and Department of Medicine, Augusta University, Augusta, Georgia, USA 11 Division of Infectious Diseases, Rady Children’s Hospital, S |
| AuthorAffiliation_xml | – name: 4 Department of Bioengineering, University of California, La Jolla, California, USA – name: 1 Division of Infectious Diseases, Department of Pediatrics, University of California, La Jolla, California, USA – name: 5 Division of Gastroenterology, Department of Pediatrics, UCSD, La Jolla, California, USA – name: 9 Skaggs School of Pharmacy and Pharmaceutical Sciences, UCSD, La Jolla, California, USA – name: 8 Department of Biology, San Diego State University, San Diego, California, USA – name: 10 Division of Pulmonary, Critical Care and Sleep Medicine, UCSD, La Jolla, California, USA – name: 6 Division of Gastroenterology, Rady Children’s Hospital, San Diego, California, USA – name: 7 Division of Host-Microbe Systems & Therapeutics, Department of Pediatrics, UC San Diego School of Medicine, La Jolla, California, USA – name: 11 Division of Infectious Diseases, Rady Children’s Hospital, San Diego, California, USA – name: 2 Immunology Center of Georgia and Department of Medicine, Augusta University, Augusta, Georgia, USA – name: 3 Glycobiology Research and Training Center, UCSD, La Jolla, California, USA |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39680460$$D View this record in MEDLINE/PubMed |
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| Snippet | The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism... The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism... |
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| SubjectTerms | Animals Antibodies, Bacterial - immunology B cells B-Lymphocytes - immunology Care and treatment Diagnosis Female Glycosylation Health aspects Humans Interleukin-10 Interleukin-10 - immunology Interleukin-10 - metabolism Mice Sialic acids Sialyltransferases - immunology Sialyltransferases - metabolism Staphylococcal Infections - immunology Staphylococcal Infections - microbiology Staphylococcal Infections - prevention & control Staphylococcal Vaccines - immunology Staphylococcus aureus - immunology Staphylococcus aureus infections STAT3 Transcription Factor - immunology STAT3 Transcription Factor - metabolism Testing Vaccination |
| Title | Pathobiont-driven antibody sialylation through IL-10 undermines vaccination |
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