Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?

Karen J. Ho; John Varga

doi:10.1016/j.jid.2017.08.017

Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?

Karen J. Ho, John Varga^*

^*Corresponding author for this work

Research output: Contribution to journal › Comment/debate › peer-review

7 Scopus citations

Abstract

Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.

Original language	English (US)
Pages (from-to)	2253-2255
Number of pages	3
Journal	Journal of Investigative Dermatology
Volume	137
Issue number	11
DOIs	https://doi.org/10.1016/j.jid.2017.08.017
State	Published - Nov 2017

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Dermatology
Cell Biology

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@article{ebb97cec3dbc4eaab62fa446348019db,

title = "Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?",

abstract = "Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.",

author = "Ho, {Karen J.} and John Varga",

note = "Funding Information: Per journal regulations, we are restricted to a limited number of references. However, many original papers are cited in the listed review articles. We acknowledge partial support by grants from National Institutes of Health (K08 HL130601 to KJH and R56 AG054207 to JV). Publisher Copyright: {\textcopyright} 2017 The Authors",

year = "2017",

month = nov,

doi = "10.1016/j.jid.2017.08.017",

language = "English (US)",

volume = "137",

pages = "2253--2255",

journal = "Journal of Investigative Dermatology",

issn = "0022-202X",

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TY - JOUR

T1 - Early-Life Gut Dysbiosis

T2 - A Driver of Later-Life Fibrosis?

AU - Ho, Karen J.

AU - Varga, John

N1 - Funding Information: Per journal regulations, we are restricted to a limited number of references. However, many original papers are cited in the listed review articles. We acknowledge partial support by grants from National Institutes of Health (K08 HL130601 to KJH and R56 AG054207 to JV). Publisher Copyright: © 2017 The Authors

PY - 2017/11

Y1 - 2017/11

N2 - Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.

AB - Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.

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U2 - 10.1016/j.jid.2017.08.017

DO - 10.1016/j.jid.2017.08.017

M3 - Comment/debate

C2 - 29055411

AN - SCOPUS:85032030983

SN - 0022-202X

VL - 137

SP - 2253

EP - 2255

JO - Journal of Investigative Dermatology

JF - Journal of Investigative Dermatology

IS - 11

ER -

Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?

Abstract

ASJC Scopus subject areas

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