Open AccessAlteration of microbiota antibody‐mediated immune selection contributes to dysbiosis in inflammatory bowel diseases
Author(s) -
Michaud Eva,
Waeckel Louis,
Gayet Rémi,
GoguyerDeschaumes Roman,
Chanut Blandine,
Jospin Fabienne,
Bathany Katell,
Monnoye Magali,
Genet Coraline,
Prier Amelie,
Tokarski Caroline,
Gérard Philippe,
Roblin Xavier,
Rochereau Nicolas,
Paul Stéphane
Publication year - 2022
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.202115386
Subject(s) - saint , library science , inflammatory bowel diseases , humanities , medicine , philosophy , art history , art , computer science , inflammatory bowel disease , pathology , disease
Human secretory immunoglobulins (SIg) A1 and SIgA2 guide mucosal responses toward tolerance or inflammation, notably through reverse‐transcytosis, the apical‐to‐basal transport of IgA2 immune complexes via M cells of gut Peyer's patches. As such, the maintenance of a diverse gut microbiota requires broad affinity IgA and glycan–glycan interaction. Here, we asked whether IgA1 and IgA2‐microbiota interactions might be involved in dysbiosis induction during inflammatory bowel diseases. Using stool HPLC‐purified IgA, we show that reverse‐transcytosis is abrogated in ulcerative colitis (UC) while it is extended to IgA1 in Crohn's disease (CD). 16S RNA sequencing of IgA‐bound microbiota in CD and UC showed distinct IgA1‐ and IgA2‐associated microbiota; the IgA1 + fraction of CD microbiota was notably enriched in beneficial commensals. These features were associated with increased IgA anti‐glycan reactivity in CD and an opposite loss of reactivity in UC. Our results highlight previously unknown pathogenic properties of IgA in IBD that could support dysbiosis.