Abstract
BackgroundChronic 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.ResultsThe 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.ConclusionsSystemic 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.
Highlights
Chronic infections have been demonstrated to maintain low-grade systemic inflammation and associate with atherosclerosis
We have recently shown in apolipoprotein E-deficient mouse model that systemic A. actinomycetemcomitans and C. pneumoniae infections may induce broad range pro-atherogenic effects including alterations in macrophage cholesterol homeostasis, endothelial function [19], and, in the liver morphology, fatty acid composition, and inflammation marker profile [20]
We focused on molecules associated with inflammation and lipid homeostasis, which were investigated on the level of gene expression and cellular fat composition
Summary
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. Recent studies have reported many site-specific physiological characteristics in AT depots, i.e. differences in cell populations, microvasculature, innervation, and regional variation in metabolic functions including adipokine profiles, lipase activities, uptake of fatty acids, and the insulin response [4]. These differences have a major impact on the proinflammatory potential of the various AT depots
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