Among older adults, age-related changes in the stool microbiome differ by HIV-1 serostatus.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 01 12 2018
revised: 14 01 2019
accepted: 14 01 2019
pubmed: 28 1 2019
medline: 27 6 2019
entrez: 28 1 2019
Statut: ppublish

Résumé

HIV-1 infection and physiological aging are independently linked to elevated systemic inflammation and changes in enteric microbial communities (dysbiosis). However, knowledge of the direct effect of HIV infection on the aging microbiome and potential links to systemic inflammation is lacking. In a cross-sectional study of older people living with HIV (PLWH) (median age 61.5 years, N = 14) and uninfected controls (median 58 years, n = 22) we compared stool microbiota, levels of microbial metabolites (short-chain fatty acid levels, SCFA) and systemic inflammatory biomarkers by HIV serostatus and age. HIV and age were independently associated with distinct changes in the stool microbiome. For example, abundances of Enterobacter and Paraprevotella were higher and Eggerthella and Roseburia lower among PLWH compared to uninfected controls. Age-related microbiome changes also differed by HIV serostatus. Some bacteria with inflammatory potential (e.g. Escherichia) increased with age among PLWH, but not controls. Stool SCFA levels were similar between the two groups yet patterns of associations between individual microbial taxa and SCFA levels differed. Abundance of various genera including Escherichia and Bifidobacterium positively associated with inflammatory biomarkers (e.g. soluble Tumor Necrosis Factor Receptors) among PLWH, but not among controls. The age effect on the gut microbiome and associations between microbiota and microbial metabolites or systemic inflammation differed based on HIV serostatus, raising important implications for the impact of therapeutic interventions, dependent on HIV serostatus or age.

Sections du résumé

BACKGROUND BACKGROUND
HIV-1 infection and physiological aging are independently linked to elevated systemic inflammation and changes in enteric microbial communities (dysbiosis). However, knowledge of the direct effect of HIV infection on the aging microbiome and potential links to systemic inflammation is lacking.
METHODS METHODS
In a cross-sectional study of older people living with HIV (PLWH) (median age 61.5 years, N = 14) and uninfected controls (median 58 years, n = 22) we compared stool microbiota, levels of microbial metabolites (short-chain fatty acid levels, SCFA) and systemic inflammatory biomarkers by HIV serostatus and age.
FINDINGS RESULTS
HIV and age were independently associated with distinct changes in the stool microbiome. For example, abundances of Enterobacter and Paraprevotella were higher and Eggerthella and Roseburia lower among PLWH compared to uninfected controls. Age-related microbiome changes also differed by HIV serostatus. Some bacteria with inflammatory potential (e.g. Escherichia) increased with age among PLWH, but not controls. Stool SCFA levels were similar between the two groups yet patterns of associations between individual microbial taxa and SCFA levels differed. Abundance of various genera including Escherichia and Bifidobacterium positively associated with inflammatory biomarkers (e.g. soluble Tumor Necrosis Factor Receptors) among PLWH, but not among controls.
INTERPRETATION CONCLUSIONS
The age effect on the gut microbiome and associations between microbiota and microbial metabolites or systemic inflammation differed based on HIV serostatus, raising important implications for the impact of therapeutic interventions, dependent on HIV serostatus or age.

Identifiants

pubmed: 30685386
pii: S2352-3964(19)30038-6
doi: 10.1016/j.ebiom.2019.01.033
pmc: PMC6413415
pii:
doi:

Substances chimiques

Biomarkers 0
Fatty Acids, Volatile 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

583-594

Subventions

Organisme : NIA NIH HHS
ID : K23 AG050260
Pays : United States
Organisme : NIA NIH HHS
ID : T32 AG000279
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002535
Pays : United States

Informations de copyright

Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.

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Auteurs

Jay Liu (J)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Rachel Johnson (R)

Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, CO, USA.

Stephanie Dillon (S)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Miranda Kroehl (M)

Department of Biostatistics and Informatics, Colorado School of Public Health, Aurora, CO, USA.

Daniel N Frank (DN)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Yunus E Tuncil (YE)

Food Engineering Department, Ordu University, Ordu, Turkey; Department of Food Science, Purdue University, Lafayette, IN, USA.

Xiaowei Zhang (X)

Department of Food Science, Purdue University, Lafayette, IN, USA.

Diana Ir (D)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Charles E Robertson (CE)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Sharon Seifert (S)

Department of Pharmacology, Children's Hospital Colorado, Aurora, CO, USA.

Janine Higgins (J)

Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.

Bruce Hamaker (B)

Department of Food Science, Purdue University, Lafayette, IN, USA.

Cara C Wilson (CC)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: cara.wilson@ucdenver.edu.

Kristine M Erlandson (KM)

Department of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. Electronic address: kristine.erlandson@ucdenver.edu.

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