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Docosahexaenoic Acid and Its Metabol...
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Yaeger, Michael Jerome,
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Docosahexaenoic Acid and Its Metabolites Protect the Lungs From Ozone-Induced Inflammation /
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Docosahexaenoic Acid and Its Metabolites Protect the Lungs From Ozone-Induced Inflammation // Michael Jerome Yaeger.
作者:
Yaeger, Michael Jerome,
面頁冊數:
1 electronic resource (122 pages)
附註:
Source: Dissertations Abstracts International, Volume: 86-11, Section: B.
Contained By:
Dissertations Abstracts International86-11B.
標題:
Toxicology. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=32112178
ISBN:
9798314893968
Docosahexaenoic Acid and Its Metabolites Protect the Lungs From Ozone-Induced Inflammation /
Yaeger, Michael Jerome,
Docosahexaenoic Acid and Its Metabolites Protect the Lungs From Ozone-Induced Inflammation /
Michael Jerome Yaeger. - 1 electronic resource (122 pages)
Source: Dissertations Abstracts International, Volume: 86-11, Section: B.
Ozone (O3) is a criteria air pollutant that increases the morbidity and mortality of pulmonary diseases such as asthma or chronic obstructive pulmonary diseases. Investigators have identified that dietary nutrients have the potential to alter the pulmonary inflammatory response to O3 exposure, potentially improving physiological outcomes. Docosahexaenoic acid (DHA) is a dietary nutrient, primarily from fish, with anti-inflammatory and pro-resolution of inflammation properties that have potential to be protective against O3-induced inflammation and injury. This is partially because DHA can be metabolized into specialized pro-resolving mediators (SPMs) that bind to receptors such as ALX/FPR2 to reduce pro-inflammatory cytokine signaling and promote resolution mechanisms. Understanding these mechanisms in the context of O3 exposure may allow for development of therapies using DHA or its metabolites to help protect people from O3-induced inflammation and injury. Chapter 1 of this dissertation provides an overview of O3-induced inflammation, DHA and its metabolites, and ALX/FPR2. Chapter 2 then investigates the role of ALX/FPR2 following O3 exposure and identifies that ALX/FPR2 is required for neutrophil recruitment through serum amyloid A signaling. Chapter 3 then describes the potential of dietary DHA to reduce O3-induced inflammation through its metabolites downregulating neutrophil recruitment by macrophages. Finally, Chapter 4 discusses the implications of these findings as well as limitations and future directions from this work.
English
ISBN: 9798314893968Subjects--Topical Terms:
556884
Toxicology.
Subjects--Index Terms:
Ozone
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Ozone (O3) is a criteria air pollutant that increases the morbidity and mortality of pulmonary diseases such as asthma or chronic obstructive pulmonary diseases. Investigators have identified that dietary nutrients have the potential to alter the pulmonary inflammatory response to O3 exposure, potentially improving physiological outcomes. Docosahexaenoic acid (DHA) is a dietary nutrient, primarily from fish, with anti-inflammatory and pro-resolution of inflammation properties that have potential to be protective against O3-induced inflammation and injury. This is partially because DHA can be metabolized into specialized pro-resolving mediators (SPMs) that bind to receptors such as ALX/FPR2 to reduce pro-inflammatory cytokine signaling and promote resolution mechanisms. Understanding these mechanisms in the context of O3 exposure may allow for development of therapies using DHA or its metabolites to help protect people from O3-induced inflammation and injury. Chapter 1 of this dissertation provides an overview of O3-induced inflammation, DHA and its metabolites, and ALX/FPR2. Chapter 2 then investigates the role of ALX/FPR2 following O3 exposure and identifies that ALX/FPR2 is required for neutrophil recruitment through serum amyloid A signaling. Chapter 3 then describes the potential of dietary DHA to reduce O3-induced inflammation through its metabolites downregulating neutrophil recruitment by macrophages. Finally, Chapter 4 discusses the implications of these findings as well as limitations and future directions from this work.
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