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Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens
A study using pair-feeding technique was conducted to determine whether heat exposure directly or indirectly (via reduced feed intake) increases intestinal mucosal damage and permeability to endotoxin in broiler chickens. Male broiler chickens (Ross 308), 27-d-old, were subjected to one of the three...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Japan Poultry Science Association
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7596036/ https://www.ncbi.nlm.nih.gov/pubmed/33132728 http://dx.doi.org/10.2141/jpsa.0190004 |
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author | Nanto-Hara, Fumika Kikusato, Motoi Ohwada, Shyuichi Toyomizu, Masaaki |
author_facet | Nanto-Hara, Fumika Kikusato, Motoi Ohwada, Shyuichi Toyomizu, Masaaki |
author_sort | Nanto-Hara, Fumika |
collection | PubMed |
description | A study using pair-feeding technique was conducted to determine whether heat exposure directly or indirectly (via reduced feed intake) increases intestinal mucosal damage and permeability to endotoxin in broiler chickens. Male broiler chickens (Ross 308), 27-d-old, were subjected to one of the three treatments (n=8): 1) thermo-neutral conditions (24°C) with ad libitum feed intake, 2) heat stress conditions (33°C) with ad libitum feed intake, or 3) pair-feeding under thermo-neutral conditions, with the feed intake identical to that of heat-stressed chickens. Using these groups, two experiments were performed to evaluate temporal changes in the intestinal morphology in response to each treatment. In experiment 1, chickens were sacrificed after 24 h of exposure to the treatment conditions, while in experiment 2, chickens were sacrificed after 12 or 72 h of exposure to the treatment conditions. In experiment 1, exposure to heat stress conditions for 24 h significantly decreased both the villus height to crypt depth ratio and number of proliferating cell nuclear antigen (PCNA)-positive cells in the duodenum and increased the plasma endotoxin concentration. These findings were not observed in pair-fed chickens. In experiment 2, intestinal integrity and function were unaffected by 12 h of heat stress. On the other hand, chickens exposed to heat stress for 72 h exhibited significantly damaged intestinal morphology in the duodenum as well as increased plasma endotoxin concentration; these negative effects were not observed in pair-fed chickens. These findings suggest that the intestinal morphology and permeability changes observed in chickens that are heat-stressed for 24–72 h are due to the heat stress conditions and not due to reduced feed intake. |
format | Online Article Text |
id | pubmed-7596036 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Japan Poultry Science Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-75960362020-10-30 Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens Nanto-Hara, Fumika Kikusato, Motoi Ohwada, Shyuichi Toyomizu, Masaaki J Poult Sci Research Note A study using pair-feeding technique was conducted to determine whether heat exposure directly or indirectly (via reduced feed intake) increases intestinal mucosal damage and permeability to endotoxin in broiler chickens. Male broiler chickens (Ross 308), 27-d-old, were subjected to one of the three treatments (n=8): 1) thermo-neutral conditions (24°C) with ad libitum feed intake, 2) heat stress conditions (33°C) with ad libitum feed intake, or 3) pair-feeding under thermo-neutral conditions, with the feed intake identical to that of heat-stressed chickens. Using these groups, two experiments were performed to evaluate temporal changes in the intestinal morphology in response to each treatment. In experiment 1, chickens were sacrificed after 24 h of exposure to the treatment conditions, while in experiment 2, chickens were sacrificed after 12 or 72 h of exposure to the treatment conditions. In experiment 1, exposure to heat stress conditions for 24 h significantly decreased both the villus height to crypt depth ratio and number of proliferating cell nuclear antigen (PCNA)-positive cells in the duodenum and increased the plasma endotoxin concentration. These findings were not observed in pair-fed chickens. In experiment 2, intestinal integrity and function were unaffected by 12 h of heat stress. On the other hand, chickens exposed to heat stress for 72 h exhibited significantly damaged intestinal morphology in the duodenum as well as increased plasma endotoxin concentration; these negative effects were not observed in pair-fed chickens. These findings suggest that the intestinal morphology and permeability changes observed in chickens that are heat-stressed for 24–72 h are due to the heat stress conditions and not due to reduced feed intake. Japan Poultry Science Association 2020-10-25 /pmc/articles/PMC7596036/ /pubmed/33132728 http://dx.doi.org/10.2141/jpsa.0190004 Text en 2020, Japan Poultry Science Association. The Journal of Poultry Science is an Open Access journal distributed under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. To view the details of this license, please visit (https://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Research Note Nanto-Hara, Fumika Kikusato, Motoi Ohwada, Shyuichi Toyomizu, Masaaki Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title | Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title_full | Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title_fullStr | Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title_full_unstemmed | Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title_short | Heat Stress Directly Affects Intestinal Integrity in Broiler Chickens |
title_sort | heat stress directly affects intestinal integrity in broiler chickens |
topic | Research Note |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7596036/ https://www.ncbi.nlm.nih.gov/pubmed/33132728 http://dx.doi.org/10.2141/jpsa.0190004 |
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