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Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature
Lyme disease (LD) infection is caused by Borrelia burgdorferi sensu lato (Bb). Due to the limited presence of this pathogen in the bloodstream in humans, diagnosis of LD relies on seroconversion. Immunoglobulins produced in response to infection are differentially glycosylated to promote or inhibit...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389449/ https://www.ncbi.nlm.nih.gov/pubmed/35990620 http://dx.doi.org/10.3389/fimmu.2022.949118 |
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author | Haslund-Gourley, Benjamin Samuel Grauzam, Stéphane Mehta, Anand S. Wigdahl, Brian Comunale, Mary Ann |
author_facet | Haslund-Gourley, Benjamin Samuel Grauzam, Stéphane Mehta, Anand S. Wigdahl, Brian Comunale, Mary Ann |
author_sort | Haslund-Gourley, Benjamin Samuel |
collection | PubMed |
description | Lyme disease (LD) infection is caused by Borrelia burgdorferi sensu lato (Bb). Due to the limited presence of this pathogen in the bloodstream in humans, diagnosis of LD relies on seroconversion. Immunoglobulins produced in response to infection are differentially glycosylated to promote or inhibit downstream inflammatory responses by the immune system. Immunoglobulin G (IgG) N-glycan responses to LD have not been characterized. In this study, we analyzed IgG N-glycans from cohorts of healthy controls, acute LD patient serum, and serum collected after acute LD patients completed a 2- to 3-week course of antibiotics and convalesced for 70-90 days. Results indicate that during the acute phase of Bb infection, IgG shifts its glycosylation profile to include structures that are not associated with the classic proinflammatory IgG N-glycan signature. This unexpected result is in direct contrast to what is reported for other inflammatory diseases. Furthermore, IgG N-glycans detected during acute LD infection discriminated between control, acute, and treated cohorts with a sensitivity of 75-100% and specificity of 94.7-100%. |
format | Online Article Text |
id | pubmed-9389449 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93894492022-08-20 Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature Haslund-Gourley, Benjamin Samuel Grauzam, Stéphane Mehta, Anand S. Wigdahl, Brian Comunale, Mary Ann Front Immunol Immunology Lyme disease (LD) infection is caused by Borrelia burgdorferi sensu lato (Bb). Due to the limited presence of this pathogen in the bloodstream in humans, diagnosis of LD relies on seroconversion. Immunoglobulins produced in response to infection are differentially glycosylated to promote or inhibit downstream inflammatory responses by the immune system. Immunoglobulin G (IgG) N-glycan responses to LD have not been characterized. In this study, we analyzed IgG N-glycans from cohorts of healthy controls, acute LD patient serum, and serum collected after acute LD patients completed a 2- to 3-week course of antibiotics and convalesced for 70-90 days. Results indicate that during the acute phase of Bb infection, IgG shifts its glycosylation profile to include structures that are not associated with the classic proinflammatory IgG N-glycan signature. This unexpected result is in direct contrast to what is reported for other inflammatory diseases. Furthermore, IgG N-glycans detected during acute LD infection discriminated between control, acute, and treated cohorts with a sensitivity of 75-100% and specificity of 94.7-100%. Frontiers Media S.A. 2022-08-05 /pmc/articles/PMC9389449/ /pubmed/35990620 http://dx.doi.org/10.3389/fimmu.2022.949118 Text en Copyright © 2022 Haslund-Gourley, Grauzam, Mehta, Wigdahl and Comunale https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Haslund-Gourley, Benjamin Samuel Grauzam, Stéphane Mehta, Anand S. Wigdahl, Brian Comunale, Mary Ann Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title | Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title_full | Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title_fullStr | Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title_full_unstemmed | Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title_short | Acute Lyme disease IgG N-linked glycans contrast the canonical inflammatory signature |
title_sort | acute lyme disease igg n-linked glycans contrast the canonical inflammatory signature |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9389449/ https://www.ncbi.nlm.nih.gov/pubmed/35990620 http://dx.doi.org/10.3389/fimmu.2022.949118 |
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