Heat stress decreases expression of the cytokines, avian β-defensins 4 and 6 and Toll-like receptor 2 in broiler chickens infected with Salmonella Enteritidis

•Relation of heat stress and Salmonella infection on chicken's immunity were assessed.•Heat stress activates HPA-axis, increasing corticosterone release.•Heat stress decreases several cytokines in Salmonella-infected chickens.•Heat stress decreases AvBD4 and 6, and TLR2 in Salmonella-infected c...

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Published inVeterinary immunology and immunopathology Vol. 186; pp. 19 - 28
Main Authors Quinteiro-Filho, W.M., Calefi, A.S., Cruz, D.S.G., Aloia, T.P.A., Zager, A., Astolfi-Ferreira, C.S., Piantino Ferreira, J.A., Sharif, S., Palermo-Neto, J.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.04.2017
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Online AccessGet full text
ISSN0165-2427
1873-2534
1873-2534
DOI10.1016/j.vetimm.2017.02.006

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Abstract •Relation of heat stress and Salmonella infection on chicken's immunity were assessed.•Heat stress activates HPA-axis, increasing corticosterone release.•Heat stress decreases several cytokines in Salmonella-infected chickens.•Heat stress decreases AvBD4 and 6, and TLR2 in Salmonella-infected chickens.•Heat stress increases Salmonella presence in crop, caecum, liver and bone marrow. A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (106cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus–pituitary–adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
AbstractList A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (106cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus–pituitary–adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (10 cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus-pituitary-adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
•Relation of heat stress and Salmonella infection on chicken's immunity were assessed.•Heat stress activates HPA-axis, increasing corticosterone release.•Heat stress decreases several cytokines in Salmonella-infected chickens.•Heat stress decreases AvBD4 and 6, and TLR2 in Salmonella-infected chickens.•Heat stress increases Salmonella presence in crop, caecum, liver and bone marrow. A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (106cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus–pituitary–adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (106cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus-pituitary-adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (106cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus-pituitary-adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
Author Sharif, S.
Cruz, D.S.G.
Piantino Ferreira, J.A.
Palermo-Neto, J.
Calefi, A.S.
Aloia, T.P.A.
Zager, A.
Astolfi-Ferreira, C.S.
Quinteiro-Filho, W.M.
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  organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil
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  organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil
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  surname: Piantino Ferreira
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28413046$$D View this record in MEDLINE/PubMed
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Keywords Salmonella
Heat stress
Cytokines
Corticosterone
Neuroimmunomodulation
Toll-like receptor
Language English
License Copyright © 2017 Elsevier B.V. All rights reserved.
cc-by-nc-nd
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PublicationTitle Veterinary immunology and immunopathology
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Snippet •Relation of heat stress and Salmonella infection on chicken's immunity were assessed.•Heat stress activates HPA-axis, increasing corticosterone release.•Heat...
A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance...
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SubjectTerms ambient temperature
animal welfare
Animals
beta-Defensins - biosynthesis
blood serum
bone marrow
Bone Marrow - microbiology
broiler chickens
cecum
Chickens
Corticosterone
Corticosterone - blood
crop (digestive system)
Cytokines
Cytokines - biosynthesis
disease resistance
gene expression
Heat stress
Heat-Shock Response
human diseases
immune response
immunoglobulin A
Immunoglobulin A - blood
Immunoglobulin G - blood
interferon-gamma
Interferon-gamma - blood
interleukin-10
interleukin-12
interleukin-1beta
interleukin-6
liver
Liver - microbiology
messenger RNA
microbial colonization
Neuroimmunomodulation
pathogens
Poultry Diseases - immunology
poultry production
Salmonella
Salmonella Enteritidis
Salmonella enteritidis - immunology
Salmonella Infections, Animal - immunology
Salmonella Infections, Animal - microbiology
salmonellosis
spleen
Spleen - immunology
Spleen - microbiology
Toll-like receptor
Toll-like receptor 2
Toll-Like Receptor 2 - biosynthesis
tonsils
transforming growth factor beta
Title Heat stress decreases expression of the cytokines, avian β-defensins 4 and 6 and Toll-like receptor 2 in broiler chickens infected with Salmonella Enteritidis
URI https://dx.doi.org/10.1016/j.vetimm.2017.02.006
https://www.ncbi.nlm.nih.gov/pubmed/28413046
https://www.proquest.com/docview/1888955392
https://www.proquest.com/docview/2000322273
http://dx.doi.org/10.1016/j.vetimm.2017.02.006
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