Title
Altered IgA response to gut bacteria is associated with childhood asthma in Peru
Date Issued
15 July 2021
Access level
open access
Resource Type
journal article
Author(s)
Hsieh C.S.
Rengarajan S.
Kau A.
Nicholson A.
Checkley W.
Romero K.
Hansel N.N.
Publisher(s)
American Association of Immunologists
Abstract
Alterations in gut microbiota in early life have been associated with the development of asthma; however, the role of gut bacteria or the IgA response to gut bacteria in school-aged children with asthma is unclear. To address this question, we profiled the microbial populations in fecal and nasal swab samples by 16S rRNA sequencing from 40 asthma and 40 control children aged 9-17 y from Peru. Clinical history and laboratory evaluation of asthma and allergy were obtained. Fecal samples were analyzed by flow cytometry and sorted into IgA+ and IgA2 subsets for 16S rRNA sequencing. We found that the fecal or nasal microbial 16S rRNA diversity and frequency of IgA+ fecal bacteria did not differ between children with or without asthma. However, the a diversity of fecal IgA+ bacteria was decreased in asthma compared with control. Machine learning analysis of fecal bacterial IgA-enrichment data revealed loss of IgA binding to the Blautia, Ruminococcus, and Lachnospiraceae taxa in children with asthma compared with controls. In addition, this loss of IgA binding was associated with worse asthma control (Asthma Control Test) and increased odds of severe as opposed to mild to moderate asthma. Thus, despite little to no change in the microbiota, children with asthma exhibit an altered host IgA response to gut bacteria compared with control participants. Notably, the signature of altered IgA responses is loss of IgA binding, in particular to members of Clostridia spp., which is associated with greater severity of asthma.
Start page
398
End page
407
Volume
207
Issue
2
Language
English
OCDE Knowledge area
Biología celular, Microbiología
Epidemiología
Scopus EID
2-s2.0-85111283100
PubMed ID
Source
Journal of Immunology
ISSN of the container
00221767
DOI of the container
10.4049/jimmunol.2001296
Sponsor(s)
This work was supported by American Asthma Association grants to C.-S.H., N.N.H., and A.K.
Sources of information:
Directorio de Producción Científica
Scopus