Bacterial but Not Fungal Gut Microbiota Alterations Are Associated With Common Variable Immunodeficiency (CVID) Phenotype

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Authors

FIEDOROVÁ Kristýna RADVANSKÝ Matěj BOSÁK Juraj GROMBIŘÍKOVÁ Hana NĚMCOVÁ Eva KRÁLÍČKOVÁ Pavlina ČERNOCHOVÁ Michaela KOTÁSKOVÁ Iva LEXA Matej LITZMAN Jiří ŠMAJS David FREIBERGER Tomáš

Year of publication 2019
Type Article in Periodical
Magazine / Source Frontiers in Immunology
MU Faculty or unit

Faculty of Medicine

Citation
Web https://www.frontiersin.org/articles/10.3389/fimmu.2019.01914/full
Doi http://dx.doi.org/10.3389/fimmu.2019.01914
Keywords CVID; IgA; gut microbiota; gut microbiome; gut mycobiota; gut mycobiome; fungal microbiota; fungal microbiome
Description Common Variable Immunodeficiency (CVID) is the most frequent symptomatic immune disorder characterized by reduced serum immunoglobulins. Patients often suffer from infectious and serious non-infectious complications which impact their life tremendously. The monogenic cause has been revealed in a minority of patients so far, indicating the role of multiple genes and environmental factors in CVID etiology. Using 16S and ITS rRNA amplicon sequencing, we analyzed the bacterial and fungal gut microbiota, respectively, in a group of 55 participants constituting of CVID patients and matched healthy controls including 16 case-control pairs living in the same household, to explore possible associations between gut microbiota composition and disease phenotype. We revealed less diverse and significantly altered bacterial but not fungal gut microbiota in CVID patients, which additionally appeared to be associated with a more severe disease phenotype. The factor of sharing the same household impacted both bacterial and fungal microbiome data significantly, although not as strongly as CVID diagnosis in bacterial assessment. Overall, our results suggest that gut bacterial microbiota is altered in CVID patients and may be one of the missing environmental drivers contributing to some of the symptoms and disease severity. Paired samples serving as controls will provide a better resolution between disease-related dysbiosis and other environmental confounders in future studies.
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