Chlamydial and Periodontal Pathogens Induce Hepatic Inflammation and Fatty Acid Imbalance in Apolipoprotein E-Deficient Mice
Autor: | Petri T. Kovanen, Anita M. Tuomainen, Saara Laitinen, Kai O. Lindros, Maija Leinonen, Reijo Käkelä, Pirkko J. Pussinen, Liisa Törmäkangas, Igor Bykov, Pekka Saikku, Kati Hyvärinen, Irma Salminen, Matti Jauhiainen, G. Alfthan |
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Rok vydání: | 2009 |
Předmět: |
Lipopolysaccharides
Male Lipopolysaccharide Immunology Inflammation Systemic inflammation medicine.disease_cause Microbiology Hepatitis Proinflammatory cytokine Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals Serum amyloid A Chlamydophila Infections Lung 030304 developmental biology Host Response and Inflammation Serum Amyloid A Protein 0303 health sciences biology Fatty Acids Aggregatibacter actinomycetemcomitans 030206 dentistry Chlamydophila pneumoniae biology.organism_classification 3. Good health Chronic infection Apolipoproteins Infectious Diseases Liver chemistry Parasitology Pasteurellaceae Pasteurellaceae Infections medicine.symptom |
Zdroj: | Infection and Immunity. 77:3442-3449 |
ISSN: | 1098-5522 0019-9567 |
DOI: | 10.1128/iai.00389-09 |
Popis: | 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. |
Databáze: | OpenAIRE |
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