title: Toll-like receptor gene expression in cecum and spleen of advanced intercross line chicks infected with Salmonella enterica serovar Enteritidis.
abstract: Understanding the changes in host gene expression that occur with bacterial infection will help to elucidate the basis of molecular genetic control of disease resistance. The effect of infecting chicks with Salmonella enterica serovar Enteritidis on the RNA expression level of Toll-like receptor (TLR) genes, and the correlation between TLR RNA expression level and bacterial burden in the cecum and spleen of young birds was studied. Chicks from two advanced intercross lines were either infected or mock infected with S. enteritidis at 1 day of age. The RNA expression levels of TLR2, TLR4 and TLR5 genes were assessed by quantitative reverse transcriptase-PCR (qRT-PCR) in cecum and spleen tissues harvested at one week post-infection. Infected chicks had significant upregulation of TLR2 RNA expression in spleen, TLR4 RNA expression in both cecum and spleen, and downregulation of TLR5 RNA expression in cecum. Bacterial burden of S. enteritidis in infected birds was not correlated with TLR RNA expression level. Infecting chicks with S. enteritidis caused an increase in TLR2, TLR4 and TLR5 RNA expression level in spleen in males but not in females. The effect of sex on response to S. enteritidis infection suggests a role for TLR signaling pathways in sex-based modulation of immune response to pathogens. High correlation between TLR2 and TLR4 mRNA expression level in cecum of S. enteritidis infected birds suggests coordinated regulation or simultaneous stimulation of these genes by S. enteritidis. In conclusion, this study clearly showed that young chicks respond to S. enteritidis infection by upregulating TLR2, TLR4 RNA expression. The downregulation of TLR5 RNA expression was observed in cecum by S. enteritidis infection, which might be beneficial to protect host cells from overstimulation by bacterial flagellin.
authors.affiliation: Department of Animal Science, 2255 Kildee Hall, Iowa State University, Ames, IA 50011, USA.
authors.forename: B
authors.initials: B
authors.lastname: Abasht
authors.forename: M G
authors.initials: MG
authors.lastname: Kaiser
authors.forename: S J
authors.initials: SJ
authors.lastname: Lamont
mesh_terms: D000818:Animals; D002432:Cecum / Q000276:immunology / Q000382:microbiology; D002645:Chickens; D003433:Crosses, Genetic; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology*; D008297:Male; D011201:Poultry Diseases / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D012481:Salmonella Infections, Animal / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D012477:Salmonella enteritidis / Q000276:immunology*; D012737:Sex Factors; D013154:Spleen / Q000276:immunology / Q000382:microbiology; D051193:Toll-Like Receptors / Q000096:biosynthesis / Q000235:genetics* / Q000276:immunology
chemical_list: D051193:Toll-Like Receptors; D012313:RNA