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Gut microbial succession follows acute secretory diarrhea in humans.

David LA, Weil A, Ryan ET, Calderwood SB, Harris JB, Chowdhury F, Begum Y, Qadri F, LaRocque RC, Turnbaugh PJ - MBio (2015)

Bottom Line: Gut bacteria may affect this recovery, but it remains incompletely understood how resident microbes in the digestive tract respond to diarrheal illness.Genomic analyses associated the succession with bacterial dispersal in food, an altered microbial environment, and changing phage levels.Our findings suggest that it may one day be feasible to manage resident bacterial populations in the gut after infectious diarrhea.

View Article: PubMed Central - PubMed

Affiliation: Society of Fellows, Harvard University, Cambridge, Massachusetts, USA FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts, USA.

No MeSH data available.


Related in: MedlinePlus

Gut microbial succession after ETEC infection. (A) To test the generalizability of the clustering model used for cholera infection (Fig. 2), a similar model was applied to longitudinal gut microbiota surveys from subjects infected with ETEC. The original Fig. 2 model was slightly modified to reflect Escherichia coli as the causal pathogen. Absent samples are labeled with an X. (B) Median group abundance levels across subjects. (C) Individual OTU abundances at each sampling date (x axis), compared to their abundances in cholera patients at corresponding times. OTUs are colored by group, with taxa that were not assigned to groups shown in gray. Spearman correlations (ρ) are shown and labeled with asterisks if P was <0.05. A pseudocount of 1e−6 has been added so that OTUs with 0 abundance can be seen.
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fig3: Gut microbial succession after ETEC infection. (A) To test the generalizability of the clustering model used for cholera infection (Fig. 2), a similar model was applied to longitudinal gut microbiota surveys from subjects infected with ETEC. The original Fig. 2 model was slightly modified to reflect Escherichia coli as the causal pathogen. Absent samples are labeled with an X. (B) Median group abundance levels across subjects. (C) Individual OTU abundances at each sampling date (x axis), compared to their abundances in cholera patients at corresponding times. OTUs are colored by group, with taxa that were not assigned to groups shown in gray. Spearman correlations (ρ) are shown and labeled with asterisks if P was <0.05. A pseudocount of 1e−6 has been added so that OTUs with 0 abundance can be seen.

Mentions: To evaluate if the groups’ dynamics after cholera could be observed with another secretory infectious diarrhea, we applied the same taxonomic model to gut microbiota from patients tracked longitudinally after infection with ETEC. To account for the causal pathogen in the ETEC cohort, we modified our taxonomic model by moving Escherichia from the Early-Stage group to the Infection-Stage group; this likely overestimated the number of infection-related bacteria at later time points, as pathogenic and commensal E. coli cannot be distinguished by 16S rRNA sequencing. With these groupings, we observed dynamics similar to the ones observed with V. cholerae infection (Fig. 3A and B). Infection-Stage and Early-Stage group bacteria were both common at 0 and 1 dpp. Late-Stage bacteria were dominant at 30 dpp. At the OTU level, there was a significant correlation between taxon abundance at 0, 1, and 30 dpp with ETEC or V. cholerae (Fig. 3C). However, we did not observe a correlation between cholera and ETEC patients’ gut microbiota at 7 dpp, midway through recovery. Although 3 of the 18 ETEC patients exhibited sizable populations of Mid-Stage group microbes at 7 dpp, this bacterial group’s median abundance was near 0 at 7 dpp. Cholera and ETEC infection therefore yielded similar microbial dynamics during the initial and late stages of recovery, but intermediate time points were pathogen specific.


Gut microbial succession follows acute secretory diarrhea in humans.

David LA, Weil A, Ryan ET, Calderwood SB, Harris JB, Chowdhury F, Begum Y, Qadri F, LaRocque RC, Turnbaugh PJ - MBio (2015)

Gut microbial succession after ETEC infection. (A) To test the generalizability of the clustering model used for cholera infection (Fig. 2), a similar model was applied to longitudinal gut microbiota surveys from subjects infected with ETEC. The original Fig. 2 model was slightly modified to reflect Escherichia coli as the causal pathogen. Absent samples are labeled with an X. (B) Median group abundance levels across subjects. (C) Individual OTU abundances at each sampling date (x axis), compared to their abundances in cholera patients at corresponding times. OTUs are colored by group, with taxa that were not assigned to groups shown in gray. Spearman correlations (ρ) are shown and labeled with asterisks if P was <0.05. A pseudocount of 1e−6 has been added so that OTUs with 0 abundance can be seen.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4442136&req=5

fig3: Gut microbial succession after ETEC infection. (A) To test the generalizability of the clustering model used for cholera infection (Fig. 2), a similar model was applied to longitudinal gut microbiota surveys from subjects infected with ETEC. The original Fig. 2 model was slightly modified to reflect Escherichia coli as the causal pathogen. Absent samples are labeled with an X. (B) Median group abundance levels across subjects. (C) Individual OTU abundances at each sampling date (x axis), compared to their abundances in cholera patients at corresponding times. OTUs are colored by group, with taxa that were not assigned to groups shown in gray. Spearman correlations (ρ) are shown and labeled with asterisks if P was <0.05. A pseudocount of 1e−6 has been added so that OTUs with 0 abundance can be seen.
Mentions: To evaluate if the groups’ dynamics after cholera could be observed with another secretory infectious diarrhea, we applied the same taxonomic model to gut microbiota from patients tracked longitudinally after infection with ETEC. To account for the causal pathogen in the ETEC cohort, we modified our taxonomic model by moving Escherichia from the Early-Stage group to the Infection-Stage group; this likely overestimated the number of infection-related bacteria at later time points, as pathogenic and commensal E. coli cannot be distinguished by 16S rRNA sequencing. With these groupings, we observed dynamics similar to the ones observed with V. cholerae infection (Fig. 3A and B). Infection-Stage and Early-Stage group bacteria were both common at 0 and 1 dpp. Late-Stage bacteria were dominant at 30 dpp. At the OTU level, there was a significant correlation between taxon abundance at 0, 1, and 30 dpp with ETEC or V. cholerae (Fig. 3C). However, we did not observe a correlation between cholera and ETEC patients’ gut microbiota at 7 dpp, midway through recovery. Although 3 of the 18 ETEC patients exhibited sizable populations of Mid-Stage group microbes at 7 dpp, this bacterial group’s median abundance was near 0 at 7 dpp. Cholera and ETEC infection therefore yielded similar microbial dynamics during the initial and late stages of recovery, but intermediate time points were pathogen specific.

Bottom Line: Gut bacteria may affect this recovery, but it remains incompletely understood how resident microbes in the digestive tract respond to diarrheal illness.Genomic analyses associated the succession with bacterial dispersal in food, an altered microbial environment, and changing phage levels.Our findings suggest that it may one day be feasible to manage resident bacterial populations in the gut after infectious diarrhea.

View Article: PubMed Central - PubMed

Affiliation: Society of Fellows, Harvard University, Cambridge, Massachusetts, USA FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts, USA.

No MeSH data available.


Related in: MedlinePlus