title: Pathway deregulation and expression QTLs in response to Actinobacillus pleuropneumoniae infection in swine.
abstract: Actinobacillus (A.) pleuropneumoniae is among the most important pathogens in pig. The agent causes severe economic losses due to decreased performance, the occurrence of acute or chronic pleuropneumonia, and an increase in death incidence. Since therapeutics cannot be used in a sustainable manner, and vaccination is not always available, new prophylactic measures are urgently needed. Recent research has provided evidence for a genetic predisposition in susceptibility to A. pleuropneumoniae in a Hampshire × German Landrace F2 family with 170 animals. The aim of the present study is to characterize the expression response in this family in order to unravel resistance and susceptibility mechanisms and to prioritize candidate genes for future fine mapping approaches. F2 pigs differed distinctly in clinical, pathological, and microbiological parameters after challenge with A. pleuropneumoniae. We monitored genome-wide gene expression from the 50 most and 50 least susceptible F2 pigs and identified 171 genes differentially expressed between these extreme phenotypes. We combined expression QTL analyses with network analyses and functional characterization using gene set enrichment analysis and identified a functional hotspot on SSC13, including 55 eQTL. The integration of the different results provides a resource for candidate prioritization for fine mapping strategies, such as TF, TFRC, RUNX1, TCN1, HP, CD14, among others.
authors.affiliation: Department of Veterinary Clinical Sciences, Justus-Liebig-University, Frankfurter Strasse 112, 35392, Giessen, Germany, gerald.reiner@vetmed.uni-giessen.de.
authors.forename: Gerald
authors.initials: G
authors.lastname: Reiner
authors.forename: Felix
authors.initials: F
authors.lastname: Dreher
authors.forename: Mario
authors.initials: M
authors.lastname: Drungowski
authors.forename: Doris
authors.initials: D
authors.lastname: Hoeltig
authors.forename: Natalie
authors.initials: N
authors.lastname: Bertsch
authors.forename: Martin
authors.initials: M
authors.lastname: Selke
authors.forename: Hermann
authors.initials: H
authors.lastname: Willems
authors.forename: Gerald Friedrich
authors.initials: GF
authors.lastname: Gerlach
authors.forename: Inga
authors.initials: I
authors.lastname: Probst
authors.forename: Burkhardt
authors.initials: B
authors.lastname: Tuemmler
authors.forename: Karl-Heinz
authors.initials: KH
authors.lastname: Waldmann
authors.forename: Ralf
authors.initials: R
authors.lastname: Herwig
mesh_terms: D000189:Actinobacillus Infections / Q000235:genetics* / Q000382:microbiology; D016977:Actinobacillus pleuropneumoniae / Q000502:physiology*; D000818:Animals; D001483:Base Sequence; D005260:Female; D005786:Gene Expression Regulation; D063990:Gene Ontology; D053263:Gene Regulatory Networks; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D054884:Host-Pathogen Interactions; D008297:Male; D011401:Promoter Regions, Genetic; D040641:Quantitative Trait Loci; D034421:Sus scrofa / Q000235:genetics; D013552:Swine; D013553:Swine Diseases / Q000235:genetics* / Q000382:microbiology; D059467:Transcriptome