Gene Expression Profiling of the Local Cecal Response of Genetic Chicken Lines That Differ in Their Susceptibility to Campylobacter jejuni Colonization
Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resista...
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Published in | PloS one Vol. 5; no. 7; p. e11827 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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28.07.2010
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Abstract | Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resistant) has less colony than line B (susceptible) on day 7 post inoculation). We hypothesize that different mechanisms between these two genetic lines may affect their ability to resist C. jejuni colonization in chickens. The molecular mechanisms of the local host response to C. jejuni colonization in chickens have not been well understood. In the present study, to profile the cecal gene expression in the response to C. jejuni colonization and to compare differences between two lines at the molecular level, RNA of ceca from two genetic lines of chickens (A and B) were applied to a chicken whole genome microarray for a pair-comparison between inoculated (I) and non-inoculated (N) chickens within each line and between lines. Our results demonstrated that metabolism process and insulin receptor signaling pathways are key contributors to the different response to C. jejuni colonization between lines A and B. With C. jejuni inoculation, lymphocyte activation and lymphoid organ development functions are important for line A host defenses, while cell differentiation, communication and signaling pathways are important for line B. Interestingly, circadian rhythm appears play a critical role in host response of the more resistant A line to C. jejuni colonization. A dramatic differential host response was observed between these two lines of chickens. The more susceptible line B chickens responded to C. jejuni inoculation with a dramatic up-regulation in lipid, glucose, and amino acid metabolism, which is undoubtedly for use in the response to the colonization with little or no change in immune host defenses. However, in more resistant line A birds the host defense responses were characterized by an up-regulation lymphocyte activation, probably by regulatory T cells and an increased expression of the NLR recognition receptor NALP1. To our knowledge, this is the first time each of these responses has been observed in the avian response to an intestinal bacterial pathogen. |
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AbstractList | Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resistant) has less colony than line B (susceptible) on day 7 post inoculation). We hypothesize that different mechanisms between these two genetic lines may affect their ability to resist C. jejuni colonization in chickens. The molecular mechanisms of the local host response to C. jejuni colonization in chickens have not been well understood. In the present study, to profile the cecal gene expression in the response to C. jejuni colonization and to compare differences between two lines at the molecular level, RNA of ceca from two genetic lines of chickens (A and B) were applied to a chicken whole genome microarray for a pair-comparison between inoculated (I) and non-inoculated (N) chickens within each line and between lines. Our results demonstrated that metabolism process and insulin receptor signaling pathways are key contributors to the different response to C. jejuni colonization between lines A and B. With C. jejuni inoculation, lymphocyte activation and lymphoid organ development functions are important for line A host defenses, while cell differentiation, communication and signaling pathways are important for line B. Interestingly, circadian rhythm appears play a critical role in host response of the more resistant A line to C. jejuni colonization. A dramatic differential host response was observed between these two lines of chickens. The more susceptible line B chickens responded to C. jejuni inoculation with a dramatic up-regulation in lipid, glucose, and amino acid metabolism, which is undoubtedly for use in the response to the colonization with little or no change in immune host defenses. However, in more resistant line A birds the host defense responses were characterized by an up-regulation lymphocyte activation, probably by regulatory T cells and an increased expression of the NLR recognition receptor NALP1. To our knowledge, this is the first time each of these responses has been observed in the avian response to an intestinal bacterial pathogen. Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resistant) has less colony than line B (susceptible) on day 7 post inoculation). We hypothesize that different mechanisms between these two genetic lines may affect their ability to resist C. jejuni colonization in chickens. The molecular mechanisms of the local host response to C. jejuni colonization in chickens have not been well understood. In the present study, to profile the cecal gene expression in the response to C. jejuni colonization and to compare differences between two lines at the molecular level, RNA of ceca from two genetic lines of chickens (A and B) were applied to a chicken whole genome microarray for a pair-comparison between inoculated (I) and non-inoculated (N) chickens within each line and between lines. Our results demonstrated that metabolism process and insulin receptor signaling pathways are key contributors to the different response to C. jejuni colonization between lines A and B. With C. jejuni inoculation, lymphocyte activation and lymphoid organ development functions are important for line A host defenses, while cell differentiation, communication and signaling pathways are important for line B. Interestingly, circadian rhythm appears play a critical role in host response of the more resistant A line to C. jejuni colonization. A dramatic differential host response was observed between these two lines of chickens. The more susceptible line B chickens responded to C. jejuni inoculation with a dramatic up-regulation in lipid, glucose, and amino acid metabolism, which is undoubtedly for use in the response to the colonization with little or no change in immune host defenses. However, in more resistant line A birds the host defense responses were characterized by an up-regulation lymphocyte activation, probably by regulatory T cells and an increased expression of the NLR recognition receptor NALP1. To our knowledge, this is the first time each of these responses has been observed in the avian response to an intestinal bacterial pathogen.Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resistant) has less colony than line B (susceptible) on day 7 post inoculation). We hypothesize that different mechanisms between these two genetic lines may affect their ability to resist C. jejuni colonization in chickens. The molecular mechanisms of the local host response to C. jejuni colonization in chickens have not been well understood. In the present study, to profile the cecal gene expression in the response to C. jejuni colonization and to compare differences between two lines at the molecular level, RNA of ceca from two genetic lines of chickens (A and B) were applied to a chicken whole genome microarray for a pair-comparison between inoculated (I) and non-inoculated (N) chickens within each line and between lines. Our results demonstrated that metabolism process and insulin receptor signaling pathways are key contributors to the different response to C. jejuni colonization between lines A and B. With C. jejuni inoculation, lymphocyte activation and lymphoid organ development functions are important for line A host defenses, while cell differentiation, communication and signaling pathways are important for line B. Interestingly, circadian rhythm appears play a critical role in host response of the more resistant A line to C. jejuni colonization. A dramatic differential host response was observed between these two lines of chickens. The more susceptible line B chickens responded to C. jejuni inoculation with a dramatic up-regulation in lipid, glucose, and amino acid metabolism, which is undoubtedly for use in the response to the colonization with little or no change in immune host defenses. However, in more resistant line A birds the host defense responses were characterized by an up-regulation lymphocyte activation, probably by regulatory T cells and an increased expression of the NLR recognition receptor NALP1. To our knowledge, this is the first time each of these responses has been observed in the avian response to an intestinal bacterial pathogen. Campylobacter jejuni ( C. jejuni ) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products. Previously, we found a significant difference in C. jejuni colonization in the ceca between two genetically distinct broiler lines (Line A (resistant) has less colony than line B (susceptible) on day 7 post inoculation). We hypothesize that different mechanisms between these two genetic lines may affect their ability to resist C. jejuni colonization in chickens. The molecular mechanisms of the local host response to C. jejuni colonization in chickens have not been well understood. In the present study, to profile the cecal gene expression in the response to C. jejuni colonization and to compare differences between two lines at the molecular level, RNA of ceca from two genetic lines of chickens (A and B) were applied to a chicken whole genome microarray for a pair-comparison between inoculated (I) and non-inoculated (N) chickens within each line and between lines. Our results demonstrated that metabolism process and insulin receptor signaling pathways are key contributors to the different response to C. jejuni colonization between lines A and B. With C. jejuni inoculation, lymphocyte activation and lymphoid organ development functions are important for line A host defenses, while cell differentiation, communication and signaling pathways are important for line B. Interestingly, circadian rhythm appears play a critical role in host response of the more resistant A line to C. jejuni colonization. A dramatic differential host response was observed between these two lines of chickens. The more susceptible line B chickens responded to C. jejuni inoculation with a dramatic up-regulation in lipid, glucose, and amino acid metabolism, which is undoubtedly for use in the response to the colonization with little or no change in immune host defenses. However, in more resistant line A birds the host defense responses were characterized by an up-regulation lymphocyte activation, probably by regulatory T cells and an increased expression of the NLR recognition receptor NALP1. To our knowledge, this is the first time each of these responses has been observed in the avian response to an intestinal bacterial pathogen. |
Audience | Academic |
Author | He, Haiqi Li, Xianyao Kogut, Michael H. Chiang, Hsin-I Genovese, Kenneth J. Wang, Ying Zhou, Huaijun Swaggerty, Christina L. |
AuthorAffiliation | 2 Southern Plains Agricultural Research Center, United States Department of Agriculture, Agricultural Research Service, College Station, Texas, United States of America Texas A&M University, United States of America 1 Department of Poultry Science, Texas A&M University, College Station, Texas, United States of America |
AuthorAffiliation_xml | – name: 2 Southern Plains Agricultural Research Center, United States Department of Agriculture, Agricultural Research Service, College Station, Texas, United States of America – name: 1 Department of Poultry Science, Texas A&M University, College Station, Texas, United States of America – name: Texas A&M University, United States of America |
Author_xml | – sequence: 1 givenname: Xianyao surname: Li fullname: Li, Xianyao – sequence: 2 givenname: Christina L. surname: Swaggerty fullname: Swaggerty, Christina L. – sequence: 3 givenname: Michael H. surname: Kogut fullname: Kogut, Michael H. – sequence: 4 givenname: Hsin-I surname: Chiang fullname: Chiang, Hsin-I – sequence: 5 givenname: Ying surname: Wang fullname: Wang, Ying – sequence: 6 givenname: Kenneth J. surname: Genovese fullname: Genovese, Kenneth J. – sequence: 7 givenname: Haiqi surname: He fullname: He, Haiqi – sequence: 8 givenname: Huaijun surname: Zhou fullname: Zhou, Huaijun |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20676366$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 Designed the microarray, provided the concepts of the study, and revised the manuscript: HZ. Carried out the microarray experiments, analyzed data and drafted the manuscript: XL. Was responsible for RNA isolation and revision of the manuscript: CLS. Contributed to data interpretation and revision of the manuscript: MHK. Assisted in sample collection, RNA isolation, array hybridization: HIC YW. Assisted in sample collection: KJG HH. |
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Snippet | Campylobacter jejuni (C. jejuni) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products.... Campylobacter jejuni ( C. jejuni ) is one of the most common causes of human bacterial enteritis worldwide primarily due to contaminated poultry products.... |
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SubjectTerms | Activation Agriculture amino acid metabolism Amino acids animal pathogenic bacteria Animals Bacteria bacterial colonization bacterial enteritis biochemical pathways Birds Campylobacter Campylobacter jejuni Campylobacter jejuni - growth & development Cecum Cecum - metabolism Cecum - microbiology Cell activation Cell differentiation Cell interactions Chickens Circadian rhythm Circadian rhythms Colonization disease resistance DNA microarrays Dressed poultry Enteritis enteropathogens Food contamination Gene expression Gene Expression Profiling gene expression regulation Genes genetic lines Genetics and Genomics/Animal Genetics Genetics and Genomics/Functional Genomics Genetics and Genomics/Gene Expression Genomes glucose Glucose metabolism host-pathogen relationships immune response Immunoregulation Inoculation Insulin Intestine lymphocyte proliferation Lymphocytes Lymphocytes T Metabolism microarray technology Molecular modelling Oligonucleotide Array Sequence Analysis Pathogens Pathways Polymerase Chain Reaction Poultry poultry products resistance mechanisms Ribonucleic acid RNA Signal transduction Signaling T cells T-lymphocytes |
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Title | Gene Expression Profiling of the Local Cecal Response of Genetic Chicken Lines That Differ in Their Susceptibility to Campylobacter jejuni Colonization |
URI | https://www.ncbi.nlm.nih.gov/pubmed/20676366 https://www.proquest.com/docview/1292424108 https://www.proquest.com/docview/2000193656 https://www.proquest.com/docview/749022214 https://www.proquest.com/docview/754556226 https://pubmed.ncbi.nlm.nih.gov/PMC2911375 https://doaj.org/article/69b3e46b979c4f14b8143d4a79032354 http://dx.doi.org/10.1371/journal.pone.0011827 |
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