What question did this study set out to answer?

This research aims to explore the connection between gut microbiota and IgA production in children with IgA deficiency and recurrent respiratory tract infections.

May 16, 2026Microbiome0 citationsOpen Access

Bifidobacterium-driven immunoglobulin A production in pediatric patients with IgA deficiency and recurrent respiratory tract infections

MKMischa H. KoenenErasmus MC MJMarien I. de JongeRadboud University Nijmegen MHMeyke HermsenRadboud University Nijmegen

Key Points

This research aims to explore the connection between gut microbiota and IgA production in children with IgA deficiency and recurrent respiratory tract infections.
Germ-free mice underwent fecal transfers from children with and without IgA deficiency.
Serum and fecal samples were taken from mice at multiple time points to measure IgA levels.
B-cell populations were collected from lung and colon tissues for analysis.
Fecal transfers induced significant increases in serum and fecal IgA levels in mice.
A Bifidobacterium cluster was linked to higher IgA levels in serum and lung tissues.
In children with rRTIs, higher Bifidobacterium abundance correlated with reduced severity of respiratory symptoms.

Abstract

BACKGROUND: Immunoglobulin A (IgA) deficiency is the most common primary antibody deficiency and contributes to recurrent respiratory tract infections (rRTIs) in children, with prevalence rates in this group ranging from 1:4 to 1:65. Previous studies in healthy humans and animals suggest that the gut microbiota significantly influences IgA production. We investigated the role of the gut microbiota in IgA deficiency and its potential in promoting IgA induction in children with rRTIs. RESULTS: 2.4%, p = 0.02). Feces from a subgroup of children with and without IgA deficiency were used to inoculate germ-free mice. At baseline and after 3, 8, 12, and 16 weeks, serum and fecal samples were collected from the mice for measurement of IgA levels and microbiota composition. We also collected B-cells from lung and colon tissues for immunohistochemistry. The introduction of microbiota in germ-free mice was related to a strong induction of serum and fecal IgA levels and associated with the abundance of specific bacterial genera, including several Lachnospiraceae species. Two community clusters were associated with fecal IgA induction, one of which was a Bifidobacterium cluster, consisting of eight bacterial genera. This Bifidobacterium cluster was also associated with higher serum and lung IgA levels and increased lung B-cell density in mice. Furthermore, in children with rRTIs, Bifidobacterium abundance was negatively associated with the severity of RTI symptoms. CONCLUSIONS: This study shows that children with IgA deficiency and rRTIs harbour a distinctly altered intestinal microbiota. Using fecal transfers from pediatric donors into germ-free mice, we demonstrate robust induction of IgA across mucosal sites. Notably, a Bifidobacterium-dominated community cluster was linked to stronger IgA responses in stool, serum, and lung, highlighting a microbiota-mucosal immunity axis with translational potential. Video Abstract.

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