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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Wiley
2021
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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) |
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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 |
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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 |
work_keys_str_mv |
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