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 in | Veterinary immunology and immunopathology Vol. 186; pp. 19 - 28 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.04.2017
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Subjects | |
Online Access | Get full text |
ISSN | 0165-2427 1873-2534 1873-2534 |
DOI | 10.1016/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 . |
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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. |
Author_xml | – sequence: 1 givenname: W.M. surname: Quinteiro-Filho fullname: Quinteiro-Filho, W.M. email: quinteirofilho@gmail.com organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 2 givenname: A.S. surname: Calefi fullname: Calefi, A.S. organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 3 givenname: D.S.G. surname: Cruz fullname: Cruz, D.S.G. organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 4 givenname: T.P.A. surname: Aloia fullname: Aloia, T.P.A. organization: Experimental Research Laboratory, Albert Einstein Jewish Institute for Education and Research, Albert Einstein Hospital, Sao Paulo, Brazil – sequence: 5 givenname: A. surname: Zager fullname: Zager, A. organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 6 givenname: C.S. surname: Astolfi-Ferreira fullname: Astolfi-Ferreira, C.S. organization: Laboratory of Avian Diseases, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 7 givenname: J.A. surname: Piantino Ferreira fullname: Piantino Ferreira, J.A. organization: Laboratory of Avian Diseases, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil – sequence: 8 givenname: S. surname: Sharif fullname: Sharif, S. organization: Laboratory of Immunology, Department of Pathobiology, University of Guelph, Guelph, ON, Canada – sequence: 9 givenname: J. surname: Palermo-Neto fullname: Palermo-Neto, J. organization: Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil |
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 |
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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 |
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