Storage conditions of high‐fat diets affect pulmonary inflammation

Abstract Obesity alters the risks and outcomes of inflammatory lung diseases. It is important to accurately recapitulate the obese state in animal models to understand these effects on the pathogenesis of disease. Diet‐induced obesity is a commonly used model of obesity, but when applied to other di...

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Autores principales: Marta Kokoszynska, Niki D. Ubags, Joseph J. Bivona III, Sebastian Ventrone, Leah F. Reed, Anne E. Dixon, Matthew J. Wargo, Matthew E. Poynter, Benjamin T. Suratt
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Publicado: Wiley 2021
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spelling oai:doaj.org-article:97e72e2c38bc4d018834a6dcd11d91812021-11-27T15:48:30ZStorage conditions of high‐fat diets affect pulmonary inflammation2051-817X10.14814/phy2.15116https://doaj.org/article/97e72e2c38bc4d018834a6dcd11d91812021-11-01T00:00:00Zhttps://doi.org/10.14814/phy2.15116https://doaj.org/toc/2051-817XAbstract Obesity alters the risks and outcomes of inflammatory lung diseases. It is important to accurately recapitulate the obese state in animal models to understand these effects on the pathogenesis of disease. Diet‐induced obesity is a commonly used model of obesity, but when applied to other disease models like acute respiratory distress syndrome, pneumonia, and asthma, it yields widely divergent. We hypothesized high‐fat chow storage conditions would affect lipid oxidation and inflammatory response in the lungs of lipopolysaccharide (LPS)‐challenged mice. For 6 weeks, C57BL/6crl mice were fed either a 10% (low‐fat diet, LFD) or 60% (high‐fat diet, HFD) stored at room temperature (RT, 23°C) for up to 7, 14, 21, or 42 days. Mice were treated with nebulized LPS to induce lung inflammation, and neutrophil levels in bronchoalveolar lavage were determined 24 h later. Lipid oxidation (malondialdehyde, MDA) was assayed by thiobarbituric acid reactive substances in chow and mouse plasma. Concentrations of MDA in chow and plasma rose in proportion to the duration of RT chow storage. Mice fed a HFD stored <2 weeks at RT had an attenuated response 24 h after LPS compared with mice fed an LFD. This effect was reversed after 2 weeks of chow storage at RT. Chow stored above freezing underwent lipid oxidation associated with significant alterations in the LPS‐induced pulmonary inflammatory response. Our data show that storage conditions affect lipid peroxidation, which in turn affects pulmonary inflammatory responses in a mouse model of disease. It also suggests changes in the microbiome, although not significantly different suggests decreased variety and richness of bacteria in the gut, a large aspect of the immune system. Dietary composition and storage of chow may also affect pulmonary inflammation and the gut microbiome in humans.Marta KokoszynskaNiki D. UbagsJoseph J. Bivona IIISebastian VentroneLeah F. ReedAnne E. DixonMatthew J. WargoMatthew E. PoynterBenjamin T. SurattWileyarticlePhysiologyQP1-981ENPhysiological Reports, Vol 9, Iss 22, Pp n/a-n/a (2021)
institution DOAJ
collection DOAJ
language EN
topic Physiology
QP1-981
spellingShingle Physiology
QP1-981
Marta Kokoszynska
Niki D. Ubags
Joseph J. Bivona III
Sebastian Ventrone
Leah F. Reed
Anne E. Dixon
Matthew J. Wargo
Matthew E. Poynter
Benjamin T. Suratt
Storage conditions of high‐fat diets affect pulmonary inflammation
description Abstract Obesity alters the risks and outcomes of inflammatory lung diseases. It is important to accurately recapitulate the obese state in animal models to understand these effects on the pathogenesis of disease. Diet‐induced obesity is a commonly used model of obesity, but when applied to other disease models like acute respiratory distress syndrome, pneumonia, and asthma, it yields widely divergent. We hypothesized high‐fat chow storage conditions would affect lipid oxidation and inflammatory response in the lungs of lipopolysaccharide (LPS)‐challenged mice. For 6 weeks, C57BL/6crl mice were fed either a 10% (low‐fat diet, LFD) or 60% (high‐fat diet, HFD) stored at room temperature (RT, 23°C) for up to 7, 14, 21, or 42 days. Mice were treated with nebulized LPS to induce lung inflammation, and neutrophil levels in bronchoalveolar lavage were determined 24 h later. Lipid oxidation (malondialdehyde, MDA) was assayed by thiobarbituric acid reactive substances in chow and mouse plasma. Concentrations of MDA in chow and plasma rose in proportion to the duration of RT chow storage. Mice fed a HFD stored <2 weeks at RT had an attenuated response 24 h after LPS compared with mice fed an LFD. This effect was reversed after 2 weeks of chow storage at RT. Chow stored above freezing underwent lipid oxidation associated with significant alterations in the LPS‐induced pulmonary inflammatory response. Our data show that storage conditions affect lipid peroxidation, which in turn affects pulmonary inflammatory responses in a mouse model of disease. It also suggests changes in the microbiome, although not significantly different suggests decreased variety and richness of bacteria in the gut, a large aspect of the immune system. Dietary composition and storage of chow may also affect pulmonary inflammation and the gut microbiome in humans.
format article
author Marta Kokoszynska
Niki D. Ubags
Joseph J. Bivona III
Sebastian Ventrone
Leah F. Reed
Anne E. Dixon
Matthew J. Wargo
Matthew E. Poynter
Benjamin T. Suratt
author_facet Marta Kokoszynska
Niki D. Ubags
Joseph J. Bivona III
Sebastian Ventrone
Leah F. Reed
Anne E. Dixon
Matthew J. Wargo
Matthew E. Poynter
Benjamin T. Suratt
author_sort Marta Kokoszynska
title Storage conditions of high‐fat diets affect pulmonary inflammation
title_short Storage conditions of high‐fat diets affect pulmonary inflammation
title_full Storage conditions of high‐fat diets affect pulmonary inflammation
title_fullStr Storage conditions of high‐fat diets affect pulmonary inflammation
title_full_unstemmed Storage conditions of high‐fat diets affect pulmonary inflammation
title_sort storage conditions of high‐fat diets affect pulmonary inflammation
publisher Wiley
publishDate 2021
url https://doaj.org/article/97e72e2c38bc4d018834a6dcd11d9181
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