High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability

Andrew M F Johnson, Anne Costanzo, Melanie Gareau, Aaron M. Armando, Oswald Quehenberger, Julie M. Jameson, Jerrold M. Olefsky

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in lep-tin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease.

Original languageEnglish (US)
Article numbere0122195
JournalPLoS One
Volume10
Issue number4
DOIs
StatePublished - Apr 2 2015

Fingerprint

High Fat Diet
high fat diet
Nutrition
eosinophils
Eosinophils
Permeability
permeability
Fats
Metabolic Diseases
mice
metabolic diseases
obesity
Obesity
tin
Tin
Macrophages
dextran
Infiltration
Gene expression
Feces

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Johnson, A. M. F., Costanzo, A., Gareau, M., Armando, A. M., Quehenberger, O., Jameson, J. M., & Olefsky, J. M. (2015). High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability. PLoS One, 10(4), [e0122195]. https://doi.org/10.1371/journal.pone.0122195

High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability. / Johnson, Andrew M F; Costanzo, Anne; Gareau, Melanie; Armando, Aaron M.; Quehenberger, Oswald; Jameson, Julie M.; Olefsky, Jerrold M.

In: PLoS One, Vol. 10, No. 4, e0122195, 02.04.2015.

Research output: Contribution to journalArticle

Johnson, AMF, Costanzo, A, Gareau, M, Armando, AM, Quehenberger, O, Jameson, JM & Olefsky, JM 2015, 'High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability', PLoS One, vol. 10, no. 4, e0122195. https://doi.org/10.1371/journal.pone.0122195
Johnson, Andrew M F ; Costanzo, Anne ; Gareau, Melanie ; Armando, Aaron M. ; Quehenberger, Oswald ; Jameson, Julie M. ; Olefsky, Jerrold M. / High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability. In: PLoS One. 2015 ; Vol. 10, No. 4.
@article{8902d2b493794efb95d667881bc0cb4f,
title = "High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability",
abstract = "The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in lep-tin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease.",
author = "Johnson, {Andrew M F} and Anne Costanzo and Melanie Gareau and Armando, {Aaron M.} and Oswald Quehenberger and Jameson, {Julie M.} and Olefsky, {Jerrold M.}",
year = "2015",
month = "4",
day = "2",
doi = "10.1371/journal.pone.0122195",
language = "English (US)",
volume = "10",
journal = "PLoS One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

TY - JOUR

T1 - High fat diet causes depletion of intestinal eosinophils associated with intestinal permeability

AU - Johnson, Andrew M F

AU - Costanzo, Anne

AU - Gareau, Melanie

AU - Armando, Aaron M.

AU - Quehenberger, Oswald

AU - Jameson, Julie M.

AU - Olefsky, Jerrold M.

PY - 2015/4/2

Y1 - 2015/4/2

N2 - The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in lep-tin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease.

AB - The development of intestinal permeability and the penetration of microbial products are key factors associated with the onset of metabolic disease. However, the mechanisms underlying this remain unclear. Here we show that, unlike liver or adipose tissue, high fat diet (HFD)/obesity in mice does not cause monocyte/macrophage infiltration into the intestine or pro-inflammatory changes in gene expression. Rather HFD causes depletion of intestinal eosinophils associated with the onset of intestinal permeability. Intestinal eosinophil numbers were restored by returning HFD fed mice to normal chow and were unchanged in lep-tin-deficient (Ob/Ob) mice, indicating that eosinophil depletion is caused specifically by a high fat diet and not obesity per se. Analysis of different aspects of intestinal permeability in HFD fed and Ob/Ob mice shows an association between eosinophil depletion and ileal paracelullar permeability, as well as leakage of albumin into the feces, but not overall permeability to FITC dextran. These findings provide the first evidence that a high fat diet causes intestinal eosinophil depletion, rather than inflammation, which may contribute to defective barrier integrity and the onset of metabolic disease.

UR - http://www.scopus.com/inward/record.url?scp=84926678423&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84926678423&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0122195

DO - 10.1371/journal.pone.0122195

M3 - Article

C2 - 25837594

AN - SCOPUS:84926678423

VL - 10

JO - PLoS One

JF - PLoS One

SN - 1932-6203

IS - 4

M1 - e0122195

ER -