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Background Interest in the interplay between host genetics and the gut microbiome in complex human diseases is increasing, with prior evidence mainly being derived from animal models. In addition, the shared and distinct microbiome features among complex human diseases remain largely unclear.
Results This analysis was based on a Chinese population with 1,475 participants. We estimated the SNP-based heritability, which suggested that Desulfovibrionaceae and Odoribacter had significant heritability estimates (0.456 and 0.476, respectively). We performed a microbiome genome-wide association study to identify host genetic variants associated with the gut microbiome. We then conducted bidirectional Mendelian randomization analyses to examine the potential causal associations between the gut microbiome and complex human diseases. We found that Saccharibacteria could potentially decrease the concentration of serum creatinine and increase the estimated glomerular filtration rate. On the other hand, atrial fibrillation, chronic kidney disease and prostate cancer, as predicted by host genetics, had potential causal effects on the abundance of some specific gut microbiota. For example, atrial fibrillation increased the abundance of Burkholderiales and Alcaligenaceae and decreased the abundance of Lachnobacterium, Bacteroides coprophilus, Barnesiellaceae, an undefined genus in the family Veillonellaceae and Mitsuokella. Further disease-microbiome feature analysis suggested that systemic lupus erythematosus and chronic myeloid leukaemia shared common gut microbiome features.
Conclusions These results suggest that different complex human diseases share common and distinct gut microbiome features, which may help reshape our understanding of disease aetiology in humans.
Keywords
Gut Microbiome, Host Genetics, Bi-directional Mendelian Randomization Analyses, Disease-Microbiome Features
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View the published article at Microbiome.
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Posted 14 Sep, 2020
No community comments so far
Editorial decision: Accept
On 11 Sep, 2020
Editor assigned
On 09 Sep, 2020
Submission checks complete
On 08 Sep, 2020
Editor invited
On 08 Sep, 2020
No comments provided
Editor assigned
On 26 Aug, 2020
Submission checks complete
On 25 Aug, 2020
Editor invited
On 25 Aug, 2020
No comments provided
Editorial decision: Minor revision
On 11 Aug, 2020
Review #2 received
Received 07 Aug, 2020
Review #1 received
Received 05 Aug, 2020
Reviewer #2 agreed
On 18 Jul, 2020
Reviewer #1 agreed
On 16 Jul, 2020
Reviewers invited
Invitations sent on 15 Jul, 2020
Editor invited
On 05 Jul, 2020
Editor assigned
On 05 Jul, 2020
Submission checks complete
On 04 Jul, 2020
First submitted
On 03 Jul, 2020
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Subject Areas
General Microbiology
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A new preprint design is coming!
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See the published version of this preprint at Microbiome.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Microbiome.
Version 3
Posted 14 Sep, 2020
No community comments so far
Editorial decision: Accept
On 11 Sep, 2020
Editor assigned
On 09 Sep, 2020
Submission checks complete
On 08 Sep, 2020
Editor invited
On 08 Sep, 2020
No comments provided
Editor assigned
On 26 Aug, 2020
Submission checks complete
On 25 Aug, 2020
Editor invited
On 25 Aug, 2020
No comments provided
Editorial decision: Minor revision
On 11 Aug, 2020
Review #2 received
Received 07 Aug, 2020
Review #1 received
Received 05 Aug, 2020
Reviewer #2 agreed
On 18 Jul, 2020
Reviewer #1 agreed
On 16 Jul, 2020
Reviewers invited
Invitations sent on 15 Jul, 2020
Editor invited
On 05 Jul, 2020
Editor assigned
On 05 Jul, 2020
Submission checks complete
On 04 Jul, 2020
First submitted
On 03 Jul, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
General Microbiology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Microbiome.
Background Interest in the interplay between host genetics and the gut microbiome in complex human diseases is increasing, with prior evidence mainly being derived from animal models. In addition, the shared and distinct microbiome features among complex human diseases remain largely unclear.
Results This analysis was based on a Chinese population with 1,475 participants. We estimated the SNP-based heritability, which suggested that Desulfovibrionaceae and Odoribacter had significant heritability estimates (0.456 and 0.476, respectively). We performed a microbiome genome-wide association study to identify host genetic variants associated with the gut microbiome. We then conducted bidirectional Mendelian randomization analyses to examine the potential causal associations between the gut microbiome and complex human diseases. We found that Saccharibacteria could potentially decrease the concentration of serum creatinine and increase the estimated glomerular filtration rate. On the other hand, atrial fibrillation, chronic kidney disease and prostate cancer, as predicted by host genetics, had potential causal effects on the abundance of some specific gut microbiota. For example, atrial fibrillation increased the abundance of Burkholderiales and Alcaligenaceae and decreased the abundance of Lachnobacterium, Bacteroides coprophilus, Barnesiellaceae, an undefined genus in the family Veillonellaceae and Mitsuokella. Further disease-microbiome feature analysis suggested that systemic lupus erythematosus and chronic myeloid leukaemia shared common gut microbiome features.
Conclusions These results suggest that different complex human diseases share common and distinct gut microbiome features, which may help reshape our understanding of disease aetiology in humans.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
The full text of this article is available to read as a PDF.
This is a list of supplementary files associated with this preprint. Click to download.
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