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The Role of the Omega-3 Polyunsatura...
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Lovins, Hannah Brooke,
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The Role of the Omega-3 Polyunsaturated Fatty Acid, Eicosapentaenoic Acid, and Its Downstream Pro-Resolving Mediators in Ozone-Induced Airspace Inflammation /
Record Type:
Electronic resources : Monograph/item
Title/Author:
The Role of the Omega-3 Polyunsaturated Fatty Acid, Eicosapentaenoic Acid, and Its Downstream Pro-Resolving Mediators in Ozone-Induced Airspace Inflammation // Hannah Brooke Lovins.
Author:
Lovins, Hannah Brooke,
Description:
1 electronic resource (145 pages)
Notes:
Source: Dissertations Abstracts International, Volume: 86-11, Section: B.
Contained By:
Dissertations Abstracts International86-11B.
Subject:
Nutrition. -
Online resource:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=32111870
ISBN:
9798314890035
The Role of the Omega-3 Polyunsaturated Fatty Acid, Eicosapentaenoic Acid, and Its Downstream Pro-Resolving Mediators in Ozone-Induced Airspace Inflammation /
Lovins, Hannah Brooke,
The Role of the Omega-3 Polyunsaturated Fatty Acid, Eicosapentaenoic Acid, and Its Downstream Pro-Resolving Mediators in Ozone-Induced Airspace Inflammation /
Hannah Brooke Lovins. - 1 electronic resource (145 pages)
Source: Dissertations Abstracts International, Volume: 86-11, Section: B.
Ambient concentrations of the air pollutant, ozone, are rising with increasing global temperatures. Ozone is known to increase incidence and exacerbation of chronic lung diseases, which will increase as ambient ozone levels rise. Studies have identified diet as a variable that is able to modulate the pulmonary health effects associated with ozone exposure. Eicosapentaenoic acid (EPA) is an n-3 (?-3) PUFA consumed through diet, which lowers inflammation through conversion to oxylipins including hydroxy-eicosapentaenoic acids (HEPEs) and the Specialized Pro-Resolving Lipid Mediator (SPM), Resolvin E1 (RvE1). We have previously shown ozone exposure downregulates expression of the RvE1 receptor, CHEMR23. RvE1 signaling through CHEMR23 drives resolution of inflammation. However, the role of dietary EPA and its downstream signaling of RvE1 and CHEMR23 in ozone-induced pulmonary inflammation is unknown. Therefore, we hypothesized that increasing dietary EPA will decrease ozone-induced pulmonary inflammation and injury through the production of HEPEs and RvE1, and that the absence of the CHEMR23 receptor will augment ozone-induced pulmonary inflammation.To test this hypothesis, we divided it into two projects. First, we utilized an EPA-supplemented diet along with 5-HEPE and 12-HEPE treatment in wildtype C57BL/6J mice to identify whether EPA supplementation leads to protection from ozone-induced pulmonary inflammation. Bronchoalveolar lavage and lung tissue were harvested and analyzed for markers of inflammation, injury, and the pulmonary lipidome. Additionally, we utilized a CHEMR23 whole-body knockout mouse model to evaluate the mechanism by which EPA inhibits ozone-induced inflammation through the RvE1/CHEMR23 signaling axis. Bronchoalveolar lavage, lung tissue, and adipose tissue were collected to measure inflammation and injury. Additionally, CHEMR23 KO bone marrow chimeras were used to evaluate the hemopoietic role of CHEMR23 signaling following ozone exposure.Together, our data indicates that an EPA-supplemented diet protects against ozone-induced airspace inflammation which is, in part, due to increasing pulmonary amounts of 5-HEPEs and 12-HEPEs. Additionally, RvE1 signaling through CHEMR23, in part, protects against ozone-induced inflammation. These findings suggest that dietary EPA in the lung can reduce ozone-driven incidences and exacerbations of chronic pulmonary diseases through metabolism to oxylipins including RvE1, which binds CHEMR23.
English
ISBN: 9798314890035Subjects--Topical Terms:
517777
Nutrition.
Subjects--Index Terms:
Eicosapentaenoic acid
The Role of the Omega-3 Polyunsaturated Fatty Acid, Eicosapentaenoic Acid, and Its Downstream Pro-Resolving Mediators in Ozone-Induced Airspace Inflammation /
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Ambient concentrations of the air pollutant, ozone, are rising with increasing global temperatures. Ozone is known to increase incidence and exacerbation of chronic lung diseases, which will increase as ambient ozone levels rise. Studies have identified diet as a variable that is able to modulate the pulmonary health effects associated with ozone exposure. Eicosapentaenoic acid (EPA) is an n-3 (?-3) PUFA consumed through diet, which lowers inflammation through conversion to oxylipins including hydroxy-eicosapentaenoic acids (HEPEs) and the Specialized Pro-Resolving Lipid Mediator (SPM), Resolvin E1 (RvE1). We have previously shown ozone exposure downregulates expression of the RvE1 receptor, CHEMR23. RvE1 signaling through CHEMR23 drives resolution of inflammation. However, the role of dietary EPA and its downstream signaling of RvE1 and CHEMR23 in ozone-induced pulmonary inflammation is unknown. Therefore, we hypothesized that increasing dietary EPA will decrease ozone-induced pulmonary inflammation and injury through the production of HEPEs and RvE1, and that the absence of the CHEMR23 receptor will augment ozone-induced pulmonary inflammation.To test this hypothesis, we divided it into two projects. First, we utilized an EPA-supplemented diet along with 5-HEPE and 12-HEPE treatment in wildtype C57BL/6J mice to identify whether EPA supplementation leads to protection from ozone-induced pulmonary inflammation. Bronchoalveolar lavage and lung tissue were harvested and analyzed for markers of inflammation, injury, and the pulmonary lipidome. Additionally, we utilized a CHEMR23 whole-body knockout mouse model to evaluate the mechanism by which EPA inhibits ozone-induced inflammation through the RvE1/CHEMR23 signaling axis. Bronchoalveolar lavage, lung tissue, and adipose tissue were collected to measure inflammation and injury. Additionally, CHEMR23 KO bone marrow chimeras were used to evaluate the hemopoietic role of CHEMR23 signaling following ozone exposure.Together, our data indicates that an EPA-supplemented diet protects against ozone-induced airspace inflammation which is, in part, due to increasing pulmonary amounts of 5-HEPEs and 12-HEPEs. Additionally, RvE1 signaling through CHEMR23, in part, protects against ozone-induced inflammation. These findings suggest that dietary EPA in the lung can reduce ozone-driven incidences and exacerbations of chronic pulmonary diseases through metabolism to oxylipins including RvE1, which binds CHEMR23.
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https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=32111870
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