Diarrhea as a Potential Cause and Consequence of Reduced Gut Microbial Diversity Among Undernourished Children in Peru.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
14 08 2020
Historique:
received: 16 03 2019
accepted: 13 09 2019
pubmed: 28 11 2019
medline: 28 4 2021
entrez: 28 11 2019
Statut: ppublish

Résumé

Detrimental effects of diarrhea on child growth and survival are well documented, but details of the underlying mechanisms remain poorly understood. Recent evidence demonstrates that perturbations to normal development of the gut microbiota in early life may contribute to growth faltering and susceptibility to related childhood diseases. We assessed associations between diarrhea, gut microbiota configuration, and childhood growth in the Peruvian Amazon. Growth, diarrhea incidence, illness, pathogen infection, and antibiotic exposure were assessed monthly in a birth cohort of 271 children aged 0-24 months. Gut bacterial diversity and abundances of specific bacterial taxa were quantified by sequencing 16S rRNA genes in fecal samples collected at 6, 12, 18, and 24 months. Linear and generalized linear models were used to determine whether diarrhea was associated with altered microbiota and, in turn, if features of the microbiota were associated with the subsequent risk of diarrhea. Diarrheal frequency, duration, and severity were negatively associated with bacterial diversity and richness (P < .05). Children born stunted (length-for-age z-score [LAZ] ≤ -2) who were also severely stunted (LAZ ≤ -3) at the time of sampling exhibited the greatest degree of diarrhea-associated reductions in bacterial diversity and the slowest recovery of bacterial diversity after episodes of diarrhea. Increased bacterial diversity was predictive of reduced subsequent diarrhea from age 6 to 18 months. Persistent, severe growth faltering may reduce the gut microbiota's resistance and resilience to diarrhea, leading to greater losses of diversity and longer recovery times. This phenotype, in turn, denotes an increased risk of future diarrheal disease and growth faltering.

Sections du résumé

BACKGROUND
Detrimental effects of diarrhea on child growth and survival are well documented, but details of the underlying mechanisms remain poorly understood. Recent evidence demonstrates that perturbations to normal development of the gut microbiota in early life may contribute to growth faltering and susceptibility to related childhood diseases. We assessed associations between diarrhea, gut microbiota configuration, and childhood growth in the Peruvian Amazon.
METHODS
Growth, diarrhea incidence, illness, pathogen infection, and antibiotic exposure were assessed monthly in a birth cohort of 271 children aged 0-24 months. Gut bacterial diversity and abundances of specific bacterial taxa were quantified by sequencing 16S rRNA genes in fecal samples collected at 6, 12, 18, and 24 months. Linear and generalized linear models were used to determine whether diarrhea was associated with altered microbiota and, in turn, if features of the microbiota were associated with the subsequent risk of diarrhea.
RESULTS
Diarrheal frequency, duration, and severity were negatively associated with bacterial diversity and richness (P < .05). Children born stunted (length-for-age z-score [LAZ] ≤ -2) who were also severely stunted (LAZ ≤ -3) at the time of sampling exhibited the greatest degree of diarrhea-associated reductions in bacterial diversity and the slowest recovery of bacterial diversity after episodes of diarrhea. Increased bacterial diversity was predictive of reduced subsequent diarrhea from age 6 to 18 months.
CONCLUSIONS
Persistent, severe growth faltering may reduce the gut microbiota's resistance and resilience to diarrhea, leading to greater losses of diversity and longer recovery times. This phenotype, in turn, denotes an increased risk of future diarrheal disease and growth faltering.

Identifiants

pubmed: 31773127
pii: 5571185
doi: 10.1093/cid/ciz905
pmc: PMC7053391
doi:

Substances chimiques

RNA, Ribosomal, 16S 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

989-999

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK056341
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.

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Auteurs

Saba Rouhani (S)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.

Nicholas W Griffin (NW)

Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine, Washington.
Center for Gut Microbiome and Nutrition Research, St. Louis, Missouri.

Pablo Peñataro Yori (PP)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
Asociación Benéfica Preferred Reporting Items for Systematic Reviews and Meta-analyses, Iquitos, Peru.

Jeanette L Gehrig (JL)

Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine, Washington.
Center for Gut Microbiome and Nutrition Research, St. Louis, Missouri.

Maribel Paredes Olortegui (MP)

Asociación Benéfica Preferred Reporting Items for Systematic Reviews and Meta-analyses, Iquitos, Peru.

Mery Siguas Salas (MS)

Asociación Benéfica Preferred Reporting Items for Systematic Reviews and Meta-analyses, Iquitos, Peru.

Dixner Rengifo Trigoso (DR)

Asociación Benéfica Preferred Reporting Items for Systematic Reviews and Meta-analyses, Iquitos, Peru.

Lawrence H Moulton (LH)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.

Eric R Houpt (ER)

University of Virginia, Charlottesville, Virginia.

Michael J Barratt (MJ)

Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine, Washington.
Center for Gut Microbiome and Nutrition Research, St. Louis, Missouri.

Margaret N Kosek (MN)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
University of Virginia, Charlottesville, Virginia.

Jeffrey I Gordon (JI)

Edison Family Center for Genome Sciences and Systems Biology, Washington University School of Medicine, Washington.
Center for Gut Microbiome and Nutrition Research, St. Louis, Missouri.

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