title: The effect of proatherogenic pathogens on adipose tissue transcriptome and fatty acid distribution in apolipoprotein E-deficient mice.
abstract: BACKGROUND
  Chronic infections have been demonstrated to maintain low-grade systemic inflammation and associate with atherosclerosis. We studied the inflammation- and lipid homeostasis-related effects of Aggregatibacter actinomycetemcomitans (Aa) and Chlamydia pneumoniae (Cpn) infections on the epididymal and inguinal adipose tissue (AT) transcriptomes and fatty acid distribution in apolipoprotein (apo) E-deficient mice. Chow-fed apoE-deficient mice were exposed to 1) chronic intranasal infection with C. pneumoniae (Cpn group), 2) recurrent intravenous infection with A. actinomycetemcomitans (Aa group), 3) a combination of both types of infection (Cpn + Aa group), or 4) infection with the vehicle (control group). Epididymal and inguinal AT gene expression was analyzed using an Illumina Mouse WG-6 v2.0 platform and quantitative PCR (QPCR). Microarray data were analyzed using Gene Ontology enrichment analysis. AT fatty acid analysis was performed using gas-liquid chromatography.
  
  
  RESULTS
  The transcriptomics data revealed significant enrichment in inflammation-associated biological pathways in both AT depots derived from the Aa and Cpn + Aa treated mice compared with the control group. The proportion of saturated fatty acids was higher in the inguinal AT in Aa (p = 0.027) and Cpn + Aa (p = 0.009) groups and in the epididymal AT in Aa group (p = 0.003). The proportion of polyunsaturated fatty acids was significantly lower among all Aa-infected groups in both depots. Chronic Cpn infection displayed only minor effects on transcriptomics and fatty acids of the AT depots.
  
  
  CONCLUSIONS
  Systemic infection with A. actinomycetemcomitans activates inflammation-related biological pathways and modulates cellular lipid homeostasis. The adverse changes in adipose tissues during chronic infection may promote atherosclerosis.
authors.affiliation: Institute of Dentistry, University of Helsinki, P,O, Box 63, 00014 Helsinki, 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: Georg
authors.initials: G
authors.lastname: Alfthan
authors.forename: Irma
authors.initials: I
authors.lastname: Salminen
authors.forename: Maija
authors.initials: M
authors.lastname: Leinonen
authors.forename: Pekka
authors.initials: P
authors.lastname: Saikku
authors.forename: Petri T
authors.initials: PT
authors.lastname: Kovanen
authors.forename: Matti
authors.initials: M
authors.lastname: Jauhiainen
authors.forename: Pirkko J
authors.initials: PJ
authors.lastname: Pussinen
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D016976:Aggregatibacter actinomycetemcomitans / Q000502:physiology*; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D050197:Atherosclerosis / Q000382:microbiology / Q000503:physiopathology; D016993:Chlamydophila pneumoniae / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism*; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D020869:Gene Expression Profiling; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D012333:RNA, Messenger / Q000378:metabolism; D059467:Transcriptome
chemical_list: D001057:Apolipoproteins E; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D012333:RNA, Messenger