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Integrating Multi-Omics and Immune P...
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Integrating Multi-Omics and Immune Profiling to Unravel the Peripartum Immune and Metabolic Changes Associated With Uterine Dysbiosis in Dairy Cows That Develop Metritis /
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Integrating Multi-Omics and Immune Profiling to Unravel the Peripartum Immune and Metabolic Changes Associated With Uterine Dysbiosis in Dairy Cows That Develop Metritis // Segundo Casaro.
作者:
Casaro, Segundo,
面頁冊數:
1 electronic resource (273 pages)
附註:
Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
Contained By:
Dissertations Abstracts International86-04B.
標題:
Neurosciences. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31334607
ISBN:
9798384469346
Integrating Multi-Omics and Immune Profiling to Unravel the Peripartum Immune and Metabolic Changes Associated With Uterine Dysbiosis in Dairy Cows That Develop Metritis /
Casaro, Segundo,
Integrating Multi-Omics and Immune Profiling to Unravel the Peripartum Immune and Metabolic Changes Associated With Uterine Dysbiosis in Dairy Cows That Develop Metritis /
Segundo Casaro. - 1 electronic resource (273 pages)
Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
The objectives of the present dissertation were to advance the understanding of metritis development in dairy cows by characterizing and integrating the peripartum systemic immune response, plasma and uterine metabolome, and the uterine microbiome. Chapter 1 introduces the main peripartum metabolic challenges cows experience and how these increase the risk for metritis development. Chapter 2 focused on designing two flow cytometry panels to characterize bovine innate and adaptative cell subpopulations. Chapter 3 used the aforementioned panels to characterize the peripartum systemic immune and metabolic changes associated with metritis. Chapter 4 focused on characterizing the peripartum plasma metabolomic changes associated with metritis. Results from Chapter 3 and 4 indicated that overconditioned cows mobilized more adipose tissue and lost more weight prepartum. To elucidate if overconditioned cows mobilized more adipose tissue because of less feed intake and energy balance, Chapter 5 focused on describing the associations between prepartum body condition score and prepartum and postpartum feed intake, energy balance, and milk production in multiparous dairy cows. Chapter 6 focused on describing the uterine environment at parturition and on the day of metritis diagnosis in cows with and without metritis. The uterine metabolome and microbiome were first characterized, and then integrated using bioinformatics to provide insights into the uterine crosstalk between opportunistic pathogenic bacteria and metabolites. Chapter 7 integrated the datasets from Chapters 3,4, and 6 using bioinformatics aiming to stablish possible causal relationships between the uterine and plasma metabolome, systemic immune response, and the uterine microbiome to advance the understanding of metritis development. Chapter 8 finalizes the dissertation with a summary of the main findings and a working hypothesis. The working hypothesis of this dissertation proposes that prepartum adiposity leads to systemic inflammation and excessive lipid mobilization prepartum. These metabolic changes lead to postpartum immune dysregulation, characterized by an excessive migration of neutrophils to the uterus but reduced mononuclear cell activation and migration, which may hinder the resolution of inflammation, potentially leading to excessive endometrial damage. Excessive tissue damage may disrupt physical barriers or increase substrate availability for bacterial growth.
English
ISBN: 9798384469346Subjects--Topical Terms:
588700
Neurosciences.
Subjects--Index Terms:
Immune function
Integrating Multi-Omics and Immune Profiling to Unravel the Peripartum Immune and Metabolic Changes Associated With Uterine Dysbiosis in Dairy Cows That Develop Metritis /
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The objectives of the present dissertation were to advance the understanding of metritis development in dairy cows by characterizing and integrating the peripartum systemic immune response, plasma and uterine metabolome, and the uterine microbiome. Chapter 1 introduces the main peripartum metabolic challenges cows experience and how these increase the risk for metritis development. Chapter 2 focused on designing two flow cytometry panels to characterize bovine innate and adaptative cell subpopulations. Chapter 3 used the aforementioned panels to characterize the peripartum systemic immune and metabolic changes associated with metritis. Chapter 4 focused on characterizing the peripartum plasma metabolomic changes associated with metritis. Results from Chapter 3 and 4 indicated that overconditioned cows mobilized more adipose tissue and lost more weight prepartum. To elucidate if overconditioned cows mobilized more adipose tissue because of less feed intake and energy balance, Chapter 5 focused on describing the associations between prepartum body condition score and prepartum and postpartum feed intake, energy balance, and milk production in multiparous dairy cows. Chapter 6 focused on describing the uterine environment at parturition and on the day of metritis diagnosis in cows with and without metritis. The uterine metabolome and microbiome were first characterized, and then integrated using bioinformatics to provide insights into the uterine crosstalk between opportunistic pathogenic bacteria and metabolites. Chapter 7 integrated the datasets from Chapters 3,4, and 6 using bioinformatics aiming to stablish possible causal relationships between the uterine and plasma metabolome, systemic immune response, and the uterine microbiome to advance the understanding of metritis development. Chapter 8 finalizes the dissertation with a summary of the main findings and a working hypothesis. The working hypothesis of this dissertation proposes that prepartum adiposity leads to systemic inflammation and excessive lipid mobilization prepartum. These metabolic changes lead to postpartum immune dysregulation, characterized by an excessive migration of neutrophils to the uterus but reduced mononuclear cell activation and migration, which may hinder the resolution of inflammation, potentially leading to excessive endometrial damage. Excessive tissue damage may disrupt physical barriers or increase substrate availability for bacterial growth.
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