title: Chlamydial and periodontal pathogens induce hepatic inflammation and fatty acid imbalance in apolipoprotein E-deficient mice.
abstract: Periodontitis and Chlamydia pneumoniae infection are independent risk factors for cardiovascular diseases. The aim of this study was to investigate the effect of C. pneumoniae and Aggregatibacter actinomycetemcomitans infection on hepatic inflammation and lipid homeostasis of apolipoprotein E-deficient mice. Mice were infected with viable C. pneumoniae intranasally three times for chronic infection or once for acute infection. Viable A. actinomycetemcomitans was administered 10 times intravenously alone or in concert with C. pneumoniae. Hepatic alterations were assessed by histochemistry, lipid quantification, and fatty acid profile analysis. The RNA expression levels and the presence of pathogens in the livers and lungs were detected by quantitative real-time PCR. Both pathogens were detected in the livers of the infected animals. Chronic C. pneumoniae infection induced marked changes in hepatic lipid homeostasis. A. actinomycetemcomitans infection resulted in inflammatory cell infiltration into the liver, accompanied by elevated hepatic RNA expression levels of inflammation-related genes and higher serum amyloid A and lipopolysaccharide concentrations. Our results indicate that proatherogenic pathogens infect the liver, causing proinflammatory alterations and lipid disturbances. This infection may maintain chronic systemic inflammation attributable to atherogenesis.
authors.affiliation: Institute of Dentistry, University of Helsinki, Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital, Finland. kati.hyvarinen@helsinki.fi
authors.forename: Kati
authors.initials: K
authors.lastname: Hyvärinen
authors.forename: Anita M
authors.initials: AM
authors.lastname: Tuomainen
authors.forename: Saara
authors.initials: S
authors.lastname: Laitinen
authors.forename: Igor L
authors.initials: IL
authors.lastname: Bykov
authors.forename: Liisa
authors.initials: L
authors.lastname: Törmäkangas
authors.forename: Kai
authors.initials: K
authors.lastname: Lindros
authors.forename: Reijo
authors.initials: R
authors.lastname: Käkelä
authors.forename: Georg
authors.initials: G
authors.lastname: Alfthan
authors.forename: Irma
authors.initials: I
authors.lastname: Salminen
authors.forename: Matti
authors.initials: M
authors.lastname: Jauhiainen
authors.forename: Petri T
authors.initials: PT
authors.lastname: Kovanen
authors.forename: Maija
authors.initials: M
authors.lastname: Leinonen
authors.forename: Pekka
authors.initials: P
authors.lastname: Saikku
authors.forename: Pirkko J
authors.initials: PJ
authors.lastname: Pussinen
mesh_terms: D000818:Animals; D001053:Apolipoproteins / Q000172:deficiency*; D023521:Chlamydophila Infections / Q000473:pathology*; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity; D005227:Fatty Acids / Q000378:metabolism*; D006505:Hepatitis / Q000382:microbiology* / Q000473:pathology*; D008070:Lipopolysaccharides / Q000097:blood; D008099:Liver / Q000382:microbiology / Q000473:pathology; D008168:Lung / Q000382:microbiology / Q000473:pathology; D008297:Male; D051379:Mice; D015661:Pasteurellaceae / Q000472:pathogenicity; D016871:Pasteurellaceae Infections / Q000473:pathology*; D000685:Serum Amyloid A Protein / Q000032:analysis
chemical_list: D001053:Apolipoproteins; D005227:Fatty Acids; D008070:Lipopolysaccharides; D000685:Serum Amyloid A Protein