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The effect of proatherogenic pathogens on adipose tissue transcriptome and fatty acid distribution in apolipoprotein E-deficient mice.

Hyvärinen K, Tuomainen AM, Laitinen S, Alfthan G, Salminen I, Leinonen M, Saikku P, Kovanen PT, Jauhiainen M, Pussinen PJ - BMC Genomics (2013)

Bottom Line: The proportion of polyunsaturated fatty acids was significantly lower among all Aa-infected groups in both depots.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Dentistry, University of Helsinki, P,O, Box 63, 00014 Helsinki, Finland. kati.hyvarinen@helsinki.fi.

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.

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The expression of de novo lipogenesis associated genes among different AT depots and infection models. The gene expression fold changes were calculated from the microarray analysis data as described in the Methods section. Differences in gene expression in the inguinal and epididymal AT transcriptomes induced by A) recurrent A. actinomycetemcomintas infection, B) chronic C. pneumoniae infection and C) combined recurrent A. actinomycetemcomintas and C. pneumoniae infections. The changes were statistically non-significant after false discovery rate correction. Acaca, acetyl-Coenzyme A carboxylase alpha; Elovl6, ELOVL family member 6, elongation of long chain fatty acids (yeast); Fasn, fatty acid synthase; Pcx, pyruvate carboxylase; Pparg, peroxisome proliferator activated receptor γ; Scd1, stearoyl-Coenzyme A desaturase 1; Scd2, stearoyl-Coenzyme A desaturase 2.
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Figure 1: The expression of de novo lipogenesis associated genes among different AT depots and infection models. The gene expression fold changes were calculated from the microarray analysis data as described in the Methods section. Differences in gene expression in the inguinal and epididymal AT transcriptomes induced by A) recurrent A. actinomycetemcomintas infection, B) chronic C. pneumoniae infection and C) combined recurrent A. actinomycetemcomintas and C. pneumoniae infections. The changes were statistically non-significant after false discovery rate correction. Acaca, acetyl-Coenzyme A carboxylase alpha; Elovl6, ELOVL family member 6, elongation of long chain fatty acids (yeast); Fasn, fatty acid synthase; Pcx, pyruvate carboxylase; Pparg, peroxisome proliferator activated receptor γ; Scd1, stearoyl-Coenzyme A desaturase 1; Scd2, stearoyl-Coenzyme A desaturase 2.

Mentions: Figure 1 presents the expression of de novo lipogenesis -associated genes in the AT depot transcriptomes among the different infection models (the data are derived from the microarray experiment). In the epididymal transcriptome of Aa-infected mice, the up-regulated genes were Pcx (FC = 2.82), fatty acid synthase (Fasn, FC = 1.81), Scd2 (FC = 2.15), and Elovl6 (FC = 3.21) (Figure 1A). Fasn and Elovl6 were down-regulated in the Cpn group in both AT depots (inguinal Fasn FC = -2.19, epididymal Fasn FC = -2.86; inguinal Elovl6 FC = -2.26, epididymal Elovl6 FC = -1.98) (Figure 1B). The combined infection model had little impact on de novo lipogenesis associated gene expression (Figure 1C).


The effect of proatherogenic pathogens on adipose tissue transcriptome and fatty acid distribution in apolipoprotein E-deficient mice.

Hyvärinen K, Tuomainen AM, Laitinen S, Alfthan G, Salminen I, Leinonen M, Saikku P, Kovanen PT, Jauhiainen M, Pussinen PJ - BMC Genomics (2013)

The expression of de novo lipogenesis associated genes among different AT depots and infection models. The gene expression fold changes were calculated from the microarray analysis data as described in the Methods section. Differences in gene expression in the inguinal and epididymal AT transcriptomes induced by A) recurrent A. actinomycetemcomintas infection, B) chronic C. pneumoniae infection and C) combined recurrent A. actinomycetemcomintas and C. pneumoniae infections. The changes were statistically non-significant after false discovery rate correction. Acaca, acetyl-Coenzyme A carboxylase alpha; Elovl6, ELOVL family member 6, elongation of long chain fatty acids (yeast); Fasn, fatty acid synthase; Pcx, pyruvate carboxylase; Pparg, peroxisome proliferator activated receptor γ; Scd1, stearoyl-Coenzyme A desaturase 1; Scd2, stearoyl-Coenzyme A desaturase 2.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4008135&req=5

Figure 1: The expression of de novo lipogenesis associated genes among different AT depots and infection models. The gene expression fold changes were calculated from the microarray analysis data as described in the Methods section. Differences in gene expression in the inguinal and epididymal AT transcriptomes induced by A) recurrent A. actinomycetemcomintas infection, B) chronic C. pneumoniae infection and C) combined recurrent A. actinomycetemcomintas and C. pneumoniae infections. The changes were statistically non-significant after false discovery rate correction. Acaca, acetyl-Coenzyme A carboxylase alpha; Elovl6, ELOVL family member 6, elongation of long chain fatty acids (yeast); Fasn, fatty acid synthase; Pcx, pyruvate carboxylase; Pparg, peroxisome proliferator activated receptor γ; Scd1, stearoyl-Coenzyme A desaturase 1; Scd2, stearoyl-Coenzyme A desaturase 2.
Mentions: Figure 1 presents the expression of de novo lipogenesis -associated genes in the AT depot transcriptomes among the different infection models (the data are derived from the microarray experiment). In the epididymal transcriptome of Aa-infected mice, the up-regulated genes were Pcx (FC = 2.82), fatty acid synthase (Fasn, FC = 1.81), Scd2 (FC = 2.15), and Elovl6 (FC = 3.21) (Figure 1A). Fasn and Elovl6 were down-regulated in the Cpn group in both AT depots (inguinal Fasn FC = -2.19, epididymal Fasn FC = -2.86; inguinal Elovl6 FC = -2.26, epididymal Elovl6 FC = -1.98) (Figure 1B). The combined infection model had little impact on de novo lipogenesis associated gene expression (Figure 1C).

Bottom Line: The proportion of polyunsaturated fatty acids was significantly lower among all Aa-infected groups in both depots.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Dentistry, University of Helsinki, P,O, Box 63, 00014 Helsinki, Finland. kati.hyvarinen@helsinki.fi.

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.

Show MeSH
Related in: MedlinePlus