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Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review

Modern livestock production became highly intensive and large scaled to increase production efficiency. This production environment could add stressors affecting the health and growth of animals. Major stressors can include environment (air quality and temperature), nutrition, and infection. These s...

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Autores principales: Lee, In Kyu, Kye, Yoon Chul, Kim, Girak, Kim, Han Wool, Gu, Min Jeong, Umboh, Johnny, Maaruf, Kartini, Kim, Sung Woo, Yun, Cheol-Heui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Asian-Australasian Association of Animal Production Societies (AAAP) and Korean Society of Animal Science and Technology (KSAST) 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932560/
https://www.ncbi.nlm.nih.gov/pubmed/27189643
http://dx.doi.org/10.5713/ajas.16.0118
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author Lee, In Kyu
Kye, Yoon Chul
Kim, Girak
Kim, Han Wool
Gu, Min Jeong
Umboh, Johnny
Maaruf, Kartini
Kim, Sung Woo
Yun, Cheol-Heui
author_facet Lee, In Kyu
Kye, Yoon Chul
Kim, Girak
Kim, Han Wool
Gu, Min Jeong
Umboh, Johnny
Maaruf, Kartini
Kim, Sung Woo
Yun, Cheol-Heui
author_sort Lee, In Kyu
collection PubMed
description Modern livestock production became highly intensive and large scaled to increase production efficiency. This production environment could add stressors affecting the health and growth of animals. Major stressors can include environment (air quality and temperature), nutrition, and infection. These stressors can reduce growth performance and alter immune systems at systemic and local levels including the gastrointestinal tract. Heat stress increases the permeability, oxidative stress, and inflammatory responses in the gut. Nutritional stress from fasting, antinutritional compounds, and toxins induces the leakage and destruction of the tight junction proteins in the gut. Fasting is shown to suppress pro-inflammatory cytokines, whereas deoxynivalenol increases the recruitment of intestinal pro-inflammatory cytokines and the level of lymphocytes in the gut. Pathogenic and viral infections such as Enterotoxigenic E. coli (ETEC) and porcine epidemic diarrhea virus can lead to loosening the intestinal epithelial barrier. On the other hand, supplementation of Lactobacillus or Saccharaomyces reduced infectious stress by ETEC. It was noted that major stressors altered the permeability of intestinal barriers and profiles of genes and proteins of pro-inflammatory cytokines and chemokines in mucosal system in pigs. However, it is not sufficient to fully explain the mechanism of the gut immune system in pigs under stress conditions. Correlation and interaction of gut and systemic immune system under major stressors should be better defined to overcome aforementioned obstacles.
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spelling pubmed-49325602016-08-01 Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review Lee, In Kyu Kye, Yoon Chul Kim, Girak Kim, Han Wool Gu, Min Jeong Umboh, Johnny Maaruf, Kartini Kim, Sung Woo Yun, Cheol-Heui Asian-Australas J Anim Sci Review Paper Modern livestock production became highly intensive and large scaled to increase production efficiency. This production environment could add stressors affecting the health and growth of animals. Major stressors can include environment (air quality and temperature), nutrition, and infection. These stressors can reduce growth performance and alter immune systems at systemic and local levels including the gastrointestinal tract. Heat stress increases the permeability, oxidative stress, and inflammatory responses in the gut. Nutritional stress from fasting, antinutritional compounds, and toxins induces the leakage and destruction of the tight junction proteins in the gut. Fasting is shown to suppress pro-inflammatory cytokines, whereas deoxynivalenol increases the recruitment of intestinal pro-inflammatory cytokines and the level of lymphocytes in the gut. Pathogenic and viral infections such as Enterotoxigenic E. coli (ETEC) and porcine epidemic diarrhea virus can lead to loosening the intestinal epithelial barrier. On the other hand, supplementation of Lactobacillus or Saccharaomyces reduced infectious stress by ETEC. It was noted that major stressors altered the permeability of intestinal barriers and profiles of genes and proteins of pro-inflammatory cytokines and chemokines in mucosal system in pigs. However, it is not sufficient to fully explain the mechanism of the gut immune system in pigs under stress conditions. Correlation and interaction of gut and systemic immune system under major stressors should be better defined to overcome aforementioned obstacles. Asian-Australasian Association of Animal Production Societies (AAAP) and Korean Society of Animal Science and Technology (KSAST) 2016-08 2016-05-12 /pmc/articles/PMC4932560/ /pubmed/27189643 http://dx.doi.org/10.5713/ajas.16.0118 Text en Copyright © 2016 by Asian-Australasian Journal of Animal Sciences This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Paper
Lee, In Kyu
Kye, Yoon Chul
Kim, Girak
Kim, Han Wool
Gu, Min Jeong
Umboh, Johnny
Maaruf, Kartini
Kim, Sung Woo
Yun, Cheol-Heui
Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title_full Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title_fullStr Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title_full_unstemmed Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title_short Stress, Nutrition, and Intestinal Immune Responses in Pigs — A Review
title_sort stress, nutrition, and intestinal immune responses in pigs — a review
topic Review Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4932560/
https://www.ncbi.nlm.nih.gov/pubmed/27189643
http://dx.doi.org/10.5713/ajas.16.0118
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