IgA—about the unexpected

Ganal‐Vonarburg, Stephanie C.

doi:10.1084/jem.20181153

Cited by 1 publication

(1 citation statement)

References 14 publications

(18 reference statements)

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“…Due to the impact the gut microbiota has on Parkinson's disease progression, and possibly the nature of the disease subtype that emerges, a fundamental question to our understanding of disease development is identifying factors that modify the gut microbiome. One possible contributor to gut microbiome changes in Parkinson's disease patients is the nature the secretory immunoglobulin A (SIgA) response to respective taxa in individuals presenting across the Parkinson's disease spectrum [14][15][16]. The collection of SIgA-coated and -uncoated taxa is referred to as the IgA-Biome and many SIgA-coated bacteria exert a homeostatic function in healthy people and are important to gut health [17,18].…”

Section: Introductionmentioning

confidence: 99%

IgA-Biome Profiles Correlate with Clinical Parkinson’s Disease Subtypes

Brown

Essigmann

Hoffman

et al. 2023

JPD

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Background: Parkinson’s disease is a heterogeneous neurodegenerative disorder with distinctive gut microbiome patterns suggesting that interventions targeting the gut microbiota may prevent, slow, or reverse disease progression and severity. Objective: Because secretory IgA (SIgA) plays a key role in shaping the gut microbiota, characterization of the IgA-Biome of individuals classified into either the akinetic rigid (AR) or tremor dominant (TD) Parkinson’s disease clinical subtypes was used to further define taxa unique to these distinct clinical phenotypes. Methods: Flow cytometry was used to separate IgA-coated and -uncoated bacteria from stool samples obtained from AR and TD patients followed by amplification and sequencing of the V4 region of the 16 S rDNA gene on the MiSeq platform (Illumina). Results: IgA-Biome analyses identified significant alpha and beta diversity differences between the Parkinson’s disease phenotypes and the Firmicutes/Bacteroides ratio was significantly higher in those with TD compared to those with AR. In addition, discriminant taxa analyses identified a more pro-inflammatory bacterial profile in the IgA + fraction of those with the AR clinical subclass compared to IgA-Biome analyses of those with the TD subclass and with the taxa identified in the unsorted control samples. Conclusion: IgA-Biome analyses underscores the importance of the host immune response in shaping the gut microbiome potentially affecting disease progression and presentation. In the present study, IgA-Biome analysis identified unique proinflammatory microbial signature in the IgA + fraction of those with AR that would have otherwise been undetected using conventional microbiome analysis approaches.

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