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Differential gene expression profiling of porcine epithelial cells infected with three enterotoxigenic Escherichia coli strains.

Zhou C, Liu Z, Jiang J, Yu Y, Zhang Q - BMC Genomics (2012)

Bottom Line: In ETEC strains, the fimbrial types F4 and F18 are commonly found differently colonized within the small intestine and cause huge economic losses in the swine industry annually worldwide.The gene ontology and pathway analysis showed that the differentially expressed genes in C(F4ab)vs control are significantly involved in cell-cycle progress and amino acid metabolism, while the clustered terms of the differentially expressed genes in C(F4ac)vs control comprise immune, inflammation and wounding response and apoptosis as well as cell cycle progress and proteolysis.The genes induced by ETECs with F4 versus F18 fimbriae suggest why ETEC with F4 may be more virulent compared to F18 which seems to elicit milder effects.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key Laboratory of Animal Genetics, Breeding and Reproduction, Ministry of Agriculture, National Engineering Laboratory for Animal Breeding, College of Animal Science and Technology, China Agricultural University, 100193 Beijing, Peoples Republic of China.

ABSTRACT

Background: Enterotoxigenic Escherichia coli (ETEC) is one of the most important pathogenic bacteria causing severe diarrhoea in human and pigs. In ETEC strains, the fimbrial types F4 and F18 are commonly found differently colonized within the small intestine and cause huge economic losses in the swine industry annually worldwide. To address the underlying mechanism, we performed a transcriptome study of porcine intestinal epithelial cells (IPEC-J2) with and without infection of three representative ETEC strains.

Results: A total 2443, 3493 and 867 differentially expressed genes were found in IPEC-J2 cells infected with F4ab ETEC (C(F4ab)), with F4ac ETEC (C(F4ac)) and with F18ac ETEC (C(F18ac)) compared to the cells without infection (control), respectively. The number of differentially expressed genes between C(F4ab) and C(F4ac), C(F4ab) and C(F18ac), and C(F4ac) and C(F18ac) were 77, 1446 and 1629, respectively. The gene ontology and pathway analysis showed that the differentially expressed genes in C(F4ab)vs control are significantly involved in cell-cycle progress and amino acid metabolism, while the clustered terms of the differentially expressed genes in C(F4ac)vs control comprise immune, inflammation and wounding response and apoptosis as well as cell cycle progress and proteolysis. Differentially expressed genes between C(F18ac)vs control are mainly involved in cell-cycle progression and immune response. Furthermore, fundamental differences were observed in expression levels of immune-related genes among the three ETEC treatments, especially for the important pro-inflammatory molecules, including IL-6, IL-8, TNF-α, CCL20, CXCL2 etc.

Conclusions: The discovery in this study provides insights into the interaction of porcine intestinal epithelial cells with F4 ETECs and F18 ETEC, respectively. The genes induced by ETECs with F4 versus F18 fimbriae suggest why ETEC with F4 may be more virulent compared to F18 which seems to elicit milder effects.

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Adhesion of the three different ETEC strains to IPEC-J2 cell monolayers as evaluated by real-time PCR. The numbers given above the columns represent means ± standard deviation. The data reported represent the mean values obtained in 3 independent experiments. Each experiment was performed in triple. P: significant level of t-test.
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Figure 4: Adhesion of the three different ETEC strains to IPEC-J2 cell monolayers as evaluated by real-time PCR. The numbers given above the columns represent means ± standard deviation. The data reported represent the mean values obtained in 3 independent experiments. Each experiment was performed in triple. P: significant level of t-test.

Mentions: As mentioned above, more immune-related genes which respond to F4ac ETEC or F4ab ETEC infection were detected in IPEC-J2 cells than those respond to F18ac ETEC infection (Figure 1D). It is probably due to the following reasons: (I) Compared to F18ac ETEC, the serotypes and virulence genes of F4ab and F4ac ETEC are more similar (Table 3). (II) Adhesion ability of the three ETECs is different. At the same time point (3 h post infection), the F4ac ETEC was the most adhesive strain, followed by F4ab ETEC with a little bit lower adhesion value (P > 0.05), whereas F18ac ETEC showed the lowest adhesion pattern compared to F4ac ETEC (Figure 4P < 0.01) and F4ab ETEC (P = 0.078). It has been reported that, in contrast to F4ac ETEC (E. coli GIS26), F18ac ETEC (E. coli 2134) has a slower colonization to the gut in vivo[38] and it does not adhere to IPEC-J2 cells [8] nor be internalized by IPEC-J2 cells in vitro[17].


Differential gene expression profiling of porcine epithelial cells infected with three enterotoxigenic Escherichia coli strains.

Zhou C, Liu Z, Jiang J, Yu Y, Zhang Q - BMC Genomics (2012)

Adhesion of the three different ETEC strains to IPEC-J2 cell monolayers as evaluated by real-time PCR. The numbers given above the columns represent means ± standard deviation. The data reported represent the mean values obtained in 3 independent experiments. Each experiment was performed in triple. P: significant level of t-test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472312&req=5

Figure 4: Adhesion of the three different ETEC strains to IPEC-J2 cell monolayers as evaluated by real-time PCR. The numbers given above the columns represent means ± standard deviation. The data reported represent the mean values obtained in 3 independent experiments. Each experiment was performed in triple. P: significant level of t-test.
Mentions: As mentioned above, more immune-related genes which respond to F4ac ETEC or F4ab ETEC infection were detected in IPEC-J2 cells than those respond to F18ac ETEC infection (Figure 1D). It is probably due to the following reasons: (I) Compared to F18ac ETEC, the serotypes and virulence genes of F4ab and F4ac ETEC are more similar (Table 3). (II) Adhesion ability of the three ETECs is different. At the same time point (3 h post infection), the F4ac ETEC was the most adhesive strain, followed by F4ab ETEC with a little bit lower adhesion value (P > 0.05), whereas F18ac ETEC showed the lowest adhesion pattern compared to F4ac ETEC (Figure 4P < 0.01) and F4ab ETEC (P = 0.078). It has been reported that, in contrast to F4ac ETEC (E. coli GIS26), F18ac ETEC (E. coli 2134) has a slower colonization to the gut in vivo[38] and it does not adhere to IPEC-J2 cells [8] nor be internalized by IPEC-J2 cells in vitro[17].

Bottom Line: In ETEC strains, the fimbrial types F4 and F18 are commonly found differently colonized within the small intestine and cause huge economic losses in the swine industry annually worldwide.The gene ontology and pathway analysis showed that the differentially expressed genes in C(F4ab)vs control are significantly involved in cell-cycle progress and amino acid metabolism, while the clustered terms of the differentially expressed genes in C(F4ac)vs control comprise immune, inflammation and wounding response and apoptosis as well as cell cycle progress and proteolysis.The genes induced by ETECs with F4 versus F18 fimbriae suggest why ETEC with F4 may be more virulent compared to F18 which seems to elicit milder effects.

View Article: PubMed Central - HTML - PubMed

Affiliation: Key Laboratory of Animal Genetics, Breeding and Reproduction, Ministry of Agriculture, National Engineering Laboratory for Animal Breeding, College of Animal Science and Technology, China Agricultural University, 100193 Beijing, Peoples Republic of China.

ABSTRACT

Background: Enterotoxigenic Escherichia coli (ETEC) is one of the most important pathogenic bacteria causing severe diarrhoea in human and pigs. In ETEC strains, the fimbrial types F4 and F18 are commonly found differently colonized within the small intestine and cause huge economic losses in the swine industry annually worldwide. To address the underlying mechanism, we performed a transcriptome study of porcine intestinal epithelial cells (IPEC-J2) with and without infection of three representative ETEC strains.

Results: A total 2443, 3493 and 867 differentially expressed genes were found in IPEC-J2 cells infected with F4ab ETEC (C(F4ab)), with F4ac ETEC (C(F4ac)) and with F18ac ETEC (C(F18ac)) compared to the cells without infection (control), respectively. The number of differentially expressed genes between C(F4ab) and C(F4ac), C(F4ab) and C(F18ac), and C(F4ac) and C(F18ac) were 77, 1446 and 1629, respectively. The gene ontology and pathway analysis showed that the differentially expressed genes in C(F4ab)vs control are significantly involved in cell-cycle progress and amino acid metabolism, while the clustered terms of the differentially expressed genes in C(F4ac)vs control comprise immune, inflammation and wounding response and apoptosis as well as cell cycle progress and proteolysis. Differentially expressed genes between C(F18ac)vs control are mainly involved in cell-cycle progression and immune response. Furthermore, fundamental differences were observed in expression levels of immune-related genes among the three ETEC treatments, especially for the important pro-inflammatory molecules, including IL-6, IL-8, TNF-α, CCL20, CXCL2 etc.

Conclusions: The discovery in this study provides insights into the interaction of porcine intestinal epithelial cells with F4 ETECs and F18 ETEC, respectively. The genes induced by ETECs with F4 versus F18 fimbriae suggest why ETEC with F4 may be more virulent compared to F18 which seems to elicit milder effects.

Show MeSH
Related in: MedlinePlus