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Investigation of Bioactive Lipids on Gut Physiology, Immune Response, and Microbiota in an In Vitro Pig Intestinal Cell Line and Neonatal Pigs Following Challenge
Investigation of Bioactive Lipids on Gut Physiology, Immune Response, and Microbiota in an...
Investigation of Bioactive Lipids on Gut Physiology, Immune Response, and Microbiota in an In Vitro Pig Intestinal Cell Line and Neonatal Pigs Following Challenge

상세정보

자료유형  
 학위논문 서양
최종처리일시  
20260202105726
ISBN  
9798270252007
DDC  
641
저자명  
Zheng, Rui.
서명/저자  
Investigation of Bioactive Lipids on Gut Physiology, Immune Response, and Microbiota in an In Vitro Pig Intestinal Cell Line and Neonatal Pigs Following Challenge
발행사항  
[Sl] : The Ohio State University, 2023
발행사항  
Ann Arbor : ProQuest Dissertations & Theses, 2023
형태사항  
188 p
주기사항  
Source: Dissertations Abstracts International, Volume: 87-07, Section: B.
주기사항  
Advisor: Jacobi, Sheila K.
학위논문주기  
Thesis (Ph.D.)--The Ohio State University, 2023.
초록/해제  
요약Optimal piglet performance is fundamental to the profitability of the swine industry. Dysregulated gut homeostasis has been associated with neurological disorders, and conversely, neurological/brain diseases can affect the gut environment. Cumulatively the nutritional, psychological, and environmental challenges early in a piglet?s life leads to increased morbidity and mortality in the swine industry. Enterotoxigenic Escherichia coli (ETEC) is a gram-negative bacterium associated with gastrointestinal (GI) disfunction and diarrhea disease in young animals worldwide, and lipopolysaccharide (LPS) also referred to as endotoxin, is a glycolipid component of its cell wall. Dietary nutrients in the early neonatal period not only provide essential sustenance for growth, but also are critical for intestinal, immunologic, and neurological development. Both long-chain polyunsaturated fatty acids (LC-PUFA) and milk fat globule membrane (MFGM) have been implicated in gut barrier function, inflammatory response, neurodevelopment, and gut microbiota. The first objective of this research is to define the local intestinal barrier function mechanisms of LC-PUFA that drive the protection of the barrier during ETEC challenge. Using the intestinal porcine epithelial cells (IPEC-J2) model, pretreatment with LC-PUFA showed various protective properties. Docosahexaenoic acid (DHA) significantly enhanced the barrier integrity by increasing transepithelial electrical resistance and decreasing fluorescein isothiocyanate-dextran flux across the epithelial barrier. Arachidonic acid (ARA) and DHA tended to increase protein abundance of membrane tight junction (TJ) protein (occludin), while increasing nuclear peroxisome proliferator-activated receptor-gamma (PPAR?). In the presence of ETEC, eicosapentaenoic acid (EPA) protected against a decline in membrane TJ claudin-1 protein. All three LC-PUFA alleviated the ETEC-induced up-regulation of nuclear factor kappa B (NF?B) p65 and decreased lactate dehydrogenase release. These results suggest that LC-PUFA protect against ETEC-induced intestinal barrier damage by regulating PPAR? and NF?B in IPEC-J2 cells. The second objective of this research is to define dietary MFGM PL mechanisms on growth performance and intestinal barrier function in neonatal piglets challenged acutely with LPS. During the suckling period, dietary MFGM had no adverse impact on growth performance or intestinal TJ proteins abundance. Dietary MFGM improved intestinal architecture by increasing villus height (VH) and villus width and decreased crypt depth (CD), thereby increasing the VH:CD ratio and villus surface. Additionally, there was an increase in colon diamine oxidase (DAO) activity with MFGM diet compared to soy-fed pigs. MFGM further resulted in interactions in mRNA expression levels of nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (I?B?), zonula occludens-1 (ZO-1), and glucagon like peptide 2 receptor (GLP-2R). These results suggest that dietary MFGM improved neonatal piglet intestinal architecture and increased colon integrity, potentially attenuating the intestinal barrier disruption following LPS challenge. The third objective is to define dietary MFGM PL mechanisms on neuroinflammatory response and gut microbiome in suckling piglets challenged acutely with LPS. Principal coordinates analysis indicated differences in microbial community structures between CON-fed and MFGM-fed groups. Dietary MFGM supplementation modulated relative abundances of several genera, including Corynebacterium, Unclassified Muribaculaceae, AM51-8, Duodenibacillus, Mediterraneibacter_A_155507, Roseburia, and Schaedlerella. Although dietary MFGM had no adverse impact on hypothalamus TJ or inflammatory cytokines at mRNA transcription level, there was an MFGM ? LPS interaction observed for I?B?. These results suggest dietary MFGM may alter neonatal piglet intestinal microbiota and marker of neuroinflammation following LPS challenge.
일반주제명  
Nutrition
일반주제명  
Animal sciences
일반주제명  
Cellular biology
일반주제명  
Immunology
키워드  
Optimal piglet performance
키워드  
Gastrointestinal disfunction
키워드  
Lipopolysaccharide
기타저자  
The Ohio State University Ohio State University Nutrition
기본자료저록  
Dissertations Abstracts International. 87-07B.
전자적 위치 및 접속  
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MARC

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■040    ▼aMiAaPQ▼cMiAaPQ
■0820  ▼a641
■1001  ▼aZheng,  Rui.
■24510▼aInvestigation  of  Bioactive  Lipids  on  Gut  Physiology,  Immune  Response,  and  Microbiota  in  an  In  Vitro  Pig  Intestinal  Cell  Line  and  Neonatal  Pigs  Following  Challenge
■260    ▼a[Sl]▼bThe  Ohio  State  University▼c2023
■260  1▼aAnn  Arbor▼bProQuest  Dissertations  &  Theses▼c2023
■300    ▼a188  p
■500    ▼aSource:  Dissertations  Abstracts  International,  Volume:  87-07,  Section:  B.
■500    ▼aAdvisor:  Jacobi,  Sheila  K.
■5021  ▼aThesis  (Ph.D.)--The  Ohio  State  University,  2023.
■520    ▼aOptimal  piglet  performance  is  fundamental  to  the  profitability  of  the  swine  industry.  Dysregulated  gut  homeostasis  has  been  associated  with  neurological  disorders,  and  conversely,  neurological
ain  diseases  can  affect  the  gut  environment.  Cumulatively  the  nutritional,  psychological,  and  environmental  challenges  early  in  a  piglet?s  life  leads  to  increased  morbidity  and  mortality  in  the  swine  industry.  Enterotoxigenic  Escherichia  coli  (ETEC)  is  a  gram-negative  bacterium  associated  with  gastrointestinal  (GI)  disfunction  and  diarrhea  disease  in  young  animals  worldwide,  and  lipopolysaccharide  (LPS)  also  referred  to  as  endotoxin,  is  a  glycolipid  component  of  its  cell  wall.  Dietary  nutrients  in  the  early  neonatal  period  not  only  provide  essential  sustenance  for  growth,  but  also  are  critical  for  intestinal,  immunologic,  and  neurological  development.  Both  long-chain  polyunsaturated  fatty  acids  (LC-PUFA)  and  milk  fat  globule  membrane  (MFGM)  have  been  implicated  in  gut  barrier  function,  inflammatory  response,  neurodevelopment,  and  gut  microbiota.            The  first  objective  of  this  research  is  to  define  the  local  intestinal  barrier  function  mechanisms  of  LC-PUFA  that  drive  the  protection  of  the  barrier  during  ETEC  challenge.  Using  the  intestinal  porcine  epithelial  cells  (IPEC-J2)  model,  pretreatment  with  LC-PUFA  showed  various  protective  properties.  Docosahexaenoic  acid  (DHA)  significantly  enhanced  the  barrier  integrity  by  increasing  transepithelial  electrical  resistance  and  decreasing  fluorescein  isothiocyanate-dextran  flux  across  the  epithelial  barrier.  Arachidonic  acid  (ARA)  and  DHA  tended  to  increase  protein  abundance  of  membrane  tight  junction  (TJ)  protein  (occludin),  while  increasing  nuclear  peroxisome  proliferator-activated  receptor-gamma  (PPAR?).  In  the  presence  of  ETEC,  eicosapentaenoic  acid  (EPA)  protected  against  a  decline  in  membrane  TJ  claudin-1  protein.  All  three  LC-PUFA  alleviated  the  ETEC-induced  up-regulation  of  nuclear  factor  kappa  B  (NF?B)  p65  and  decreased  lactate  dehydrogenase  release.  These  results  suggest  that  LC-PUFA  protect  against  ETEC-induced  intestinal  barrier  damage  by  regulating  PPAR?  and  NF?B  in  IPEC-J2  cells.            The  second  objective  of  this  research  is  to  define  dietary  MFGM  PL  mechanisms  on  growth  performance  and  intestinal  barrier  function  in  neonatal  piglets  challenged  acutely  with  LPS.  During  the  suckling  period,  dietary  MFGM  had  no  adverse  impact  on  growth  performance  or  intestinal  TJ  proteins  abundance.  Dietary  MFGM  improved  intestinal  architecture  by  increasing  villus  height  (VH)  and  villus  width  and  decreased  crypt  depth  (CD),  thereby  increasing  the  VH:CD  ratio  and  villus  surface.  Additionally,  there  was  an  increase  in  colon  diamine  oxidase  (DAO)  activity  with  MFGM  diet  compared  to  soy-fed  pigs.  MFGM  further  resulted  in  interactions  in  mRNA  expression  levels  of  nuclear  factor  of  kappa  light  polypeptide  gene  enhancer  in  B  cells  inhibitor  alpha  (I?B?),  zonula  occludens-1  (ZO-1),  and  glucagon  like  peptide  2  receptor  (GLP-2R).  These  results  suggest  that  dietary  MFGM  improved  neonatal  piglet  intestinal  architecture  and  increased  colon  integrity,  potentially  attenuating  the  intestinal  barrier  disruption  following  LPS  challenge.            The  third  objective  is  to  define  dietary  MFGM  PL  mechanisms  on  neuroinflammatory  response  and  gut  microbiome  in  suckling  piglets  challenged  acutely  with  LPS.  Principal  coordinates  analysis  indicated  differences  in  microbial  community  structures  between  CON-fed  and  MFGM-fed  groups.  Dietary  MFGM  supplementation  modulated  relative  abundances  of  several  genera,  including  Corynebacterium,  Unclassified  Muribaculaceae,  AM51-8,  Duodenibacillus,  Mediterraneibacter_A_155507,  Roseburia,  and  Schaedlerella.  Although  dietary  MFGM  had  no  adverse  impact  on  hypothalamus  TJ  or  inflammatory  cytokines  at  mRNA  transcription  level,  there  was  an  MFGM  ?  LPS  interaction  observed  for  I?B?.  These  results  suggest  dietary  MFGM  may  alter  neonatal  piglet  intestinal  microbiota  and  marker  of  neuroinflammation  following  LPS  challenge.
■590    ▼aSchool  code:  0168.
■650  4▼aNutrition
■650  4▼aAnimal  sciences
■650  4▼aCellular  biology
■650  4▼aImmunology
■653    ▼aOptimal  piglet  performance
■653    ▼aGastrointestinal  disfunction
■653    ▼aLipopolysaccharide
■690    ▼a0570
■690    ▼a0475
■690    ▼a0379
■690    ▼a0982
■71020▼aThe  Ohio  State  University▼bOhio  State  University  Nutrition.
■7730  ▼tDissertations  Abstracts  International▼g87-07B.
■790    ▼a0168
■791    ▼aPh.D.
■792    ▼a2023
■793    ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17361280▼nKERIS▼z이  자료의  원문은  한국교육학술정보원에서  제공합니다.

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