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Infection with the gastrointestinal nematode Ostertagia ostertagi in cattle affects mucus biosynthesis in the abomasum.

Rinaldi M, Dreesen L, Hoorens PR, Li RW, Claerebout E, Goddeeris B, Vercruysse J, Van Den Broek W, Geldhof P - Vet. Res. (2011)

Bottom Line: Several genes involved in mucin core structure synthesis, branching and oligomerization, such as GCNT3, GCNT4, A4GNT and protein disulphide isomerases were found to be upregulated.Finally, transcription levels of 2 trefoil factors, TFF1 and TFF3, which are co-expressed with mucins in the GI tract, were also found to be significantly upregulated in infected animals.Although the alterations in mucus biosynthesis started early during infection, the biggest effects were found when adult worms were present on the surface of the abomasal mucosa and are likely caused by the alterations in mucosal cell populations, characterized by hyperplasia of mucus secreting cells.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. peter.geldhof@UGent.be.

ABSTRACT
The mucus layer in the gastrointestinal (GI) tract is considered to be the first line of defense to the external environment. Alteration in mucus components has been reported to occur during intestinal nematode infection in ruminants, but the role of mucus in response to abomasal parasites remains largely unclear. The aim of the current study was to analyze the effects of an Ostertagia ostertagi infection on the abomasal mucus biosynthesis in cattle. Increased gene expression of MUC1, MUC6 and MUC20 was observed, while MUC5AC did not change during infection. Qualitative changes of mucins, related to sugar composition, were also observed. AB-PAS and HID-AB stainings highlighted a decrease in neutral and an increase in acidic mucins, throughout the infection. Several genes involved in mucin core structure synthesis, branching and oligomerization, such as GCNT3, GCNT4, A4GNT and protein disulphide isomerases were found to be upregulated. Increase in mucin fucosylation was observed using the lectin UEA-I and through the evaluation of fucosyltransferases gene expression levels. Finally, transcription levels of 2 trefoil factors, TFF1 and TFF3, which are co-expressed with mucins in the GI tract, were also found to be significantly upregulated in infected animals. Although the alterations in mucus biosynthesis started early during infection, the biggest effects were found when adult worms were present on the surface of the abomasal mucosa and are likely caused by the alterations in mucosal cell populations, characterized by hyperplasia of mucus secreting cells.

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Lectin staining with UEAI (a-L-Fucosyl terminals). Carnoy's fixed, paraffin-embedded abomasum sections of Holstein cows after Ostertagia ostertagi infection were stained. (A and C) negative control, (B and D) exposed to O. ostertagi for 21 days. Original magnification 20× (left panels), 40× (right panels).
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Figure 3: Lectin staining with UEAI (a-L-Fucosyl terminals). Carnoy's fixed, paraffin-embedded abomasum sections of Holstein cows after Ostertagia ostertagi infection were stained. (A and C) negative control, (B and D) exposed to O. ostertagi for 21 days. Original magnification 20× (left panels), 40× (right panels).

Mentions: To study alterations in the saccharide residues on mucins, 6 lectins were used to stain the abomasal mucosa of control (0 dpi) and infected (14, 21 dpi and 60 dpe) animals (Table 1). Both the secreted mucus and the mucus producing cells (SMCs and MNCs) of healthy animals were strongly (++) stained by WGA, which binds N-acetyl glucosamine and by RCA120, DBA, SBA and PNA, which all have high affinity for galactose and N-acetylgalactosamine residues (Table 2). UEA-I, a lectin with affinity for L-fucose, stained the MNCs (++) intensely in uninfected animals whereas SMCs were not stained (-) and the secreted mucus only stained weakly (+/-) (Table 2). The staining pattern of only two lectins was found to be modified after an O. ostertagi infection. UEA-I (for L-Fuc) showed an increased staining of secreted mucus and SMCs at 21 dpi (Figure 3b and 3d) and 60 dpe (Figure 3a and 3c). Conversely, PNA staining (for Gal and GalNAc) was decreased at 21 dpi in secreted mucus, SMCs and MNCs (Table 2). The other lectins did not seem to give an altered staining during infection (Table 2).


Infection with the gastrointestinal nematode Ostertagia ostertagi in cattle affects mucus biosynthesis in the abomasum.

Rinaldi M, Dreesen L, Hoorens PR, Li RW, Claerebout E, Goddeeris B, Vercruysse J, Van Den Broek W, Geldhof P - Vet. Res. (2011)

Lectin staining with UEAI (a-L-Fucosyl terminals). Carnoy's fixed, paraffin-embedded abomasum sections of Holstein cows after Ostertagia ostertagi infection were stained. (A and C) negative control, (B and D) exposed to O. ostertagi for 21 days. Original magnification 20× (left panels), 40× (right panels).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3102617&req=5

Figure 3: Lectin staining with UEAI (a-L-Fucosyl terminals). Carnoy's fixed, paraffin-embedded abomasum sections of Holstein cows after Ostertagia ostertagi infection were stained. (A and C) negative control, (B and D) exposed to O. ostertagi for 21 days. Original magnification 20× (left panels), 40× (right panels).
Mentions: To study alterations in the saccharide residues on mucins, 6 lectins were used to stain the abomasal mucosa of control (0 dpi) and infected (14, 21 dpi and 60 dpe) animals (Table 1). Both the secreted mucus and the mucus producing cells (SMCs and MNCs) of healthy animals were strongly (++) stained by WGA, which binds N-acetyl glucosamine and by RCA120, DBA, SBA and PNA, which all have high affinity for galactose and N-acetylgalactosamine residues (Table 2). UEA-I, a lectin with affinity for L-fucose, stained the MNCs (++) intensely in uninfected animals whereas SMCs were not stained (-) and the secreted mucus only stained weakly (+/-) (Table 2). The staining pattern of only two lectins was found to be modified after an O. ostertagi infection. UEA-I (for L-Fuc) showed an increased staining of secreted mucus and SMCs at 21 dpi (Figure 3b and 3d) and 60 dpe (Figure 3a and 3c). Conversely, PNA staining (for Gal and GalNAc) was decreased at 21 dpi in secreted mucus, SMCs and MNCs (Table 2). The other lectins did not seem to give an altered staining during infection (Table 2).

Bottom Line: Several genes involved in mucin core structure synthesis, branching and oligomerization, such as GCNT3, GCNT4, A4GNT and protein disulphide isomerases were found to be upregulated.Finally, transcription levels of 2 trefoil factors, TFF1 and TFF3, which are co-expressed with mucins in the GI tract, were also found to be significantly upregulated in infected animals.Although the alterations in mucus biosynthesis started early during infection, the biggest effects were found when adult worms were present on the surface of the abomasal mucosa and are likely caused by the alterations in mucosal cell populations, characterized by hyperplasia of mucus secreting cells.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Virology, Parasitology and Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820 Merelbeke, Belgium. peter.geldhof@UGent.be.

ABSTRACT
The mucus layer in the gastrointestinal (GI) tract is considered to be the first line of defense to the external environment. Alteration in mucus components has been reported to occur during intestinal nematode infection in ruminants, but the role of mucus in response to abomasal parasites remains largely unclear. The aim of the current study was to analyze the effects of an Ostertagia ostertagi infection on the abomasal mucus biosynthesis in cattle. Increased gene expression of MUC1, MUC6 and MUC20 was observed, while MUC5AC did not change during infection. Qualitative changes of mucins, related to sugar composition, were also observed. AB-PAS and HID-AB stainings highlighted a decrease in neutral and an increase in acidic mucins, throughout the infection. Several genes involved in mucin core structure synthesis, branching and oligomerization, such as GCNT3, GCNT4, A4GNT and protein disulphide isomerases were found to be upregulated. Increase in mucin fucosylation was observed using the lectin UEA-I and through the evaluation of fucosyltransferases gene expression levels. Finally, transcription levels of 2 trefoil factors, TFF1 and TFF3, which are co-expressed with mucins in the GI tract, were also found to be significantly upregulated in infected animals. Although the alterations in mucus biosynthesis started early during infection, the biggest effects were found when adult worms were present on the surface of the abomasal mucosa and are likely caused by the alterations in mucosal cell populations, characterized by hyperplasia of mucus secreting cells.

Show MeSH
Related in: MedlinePlus