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Mucin and galectin dynamics during gastro-intestinal parasite infections in cattle

Prisca Hoorens UGent (2011)
abstract
Gastro-intestinal (GI) nematodes are an important cause of disease and economical loss in livestock industries. The abomasal nematode Ostertagia ostertagi and the intestinal nematode Cooperia oncophora are among the most common parasites infecting cattle in temperate climate regions. In order to develop new therapeutics, a fundamental understanding of the processes involved in protective immunity is needed. The potential role of mucins and other defensive compounds (trefoil factors/TFF and galectins/LGALS) is described. Nine membrane-bound and six secreted mucins were identified in the bovine genome. The protein architecture of the membrane bound mucins was similar between humans and cattle, while the protein architecture of the gel forming mucins seemed less conserved. The transcriptional distribution of both mucins and mucin glycosyltransferases was investigated in the GI tract of nematode-free cattle. Both sets of genes showed a tissuespecific transcritpion profile and species-specific differences were also observed. Subsequently, changes in the transcription of mucins, mucin glycosyltransferases and TFFs were investigated in the abomasal mucosa during primary and repeated infections with O. ostertagi. This study showed that the mucin, TFF and glycosyltransferase transcription levels were significantly altered in the abomasal mucosa during primary O. ostertagi infection in cattle. Although the changes in mucin biosynthesis started early after infection, the major effects were observed when adult worms were present at the mucosal surface. In addition, the transcriptional distribution of ten galectins was investigated in the GI tract of uninfected cattle. The majority of the galectins were upregulated at an early time point after infection, before the appearance of adult worms. LGALS1 was also upregulated in repeatedly infected animals, possible indication that it might be involved in the development of protective immunity. LGALS11 was inducibly and strongly upregulated during both primary and repeated infections with O. ostertagi. The changes in these components in the abomasum during O. ostertagi infections were compared with changes in the small intestine after primary and repeated infections with C. oncophora. The identification of components that are commonly or differentially induced during O. ostertagi and C. oncophora infections might be useful to identify mechanisms involved in protection. For some glycosyltransferases and galectins, differences were observed in the changes in transcription levels. Other molecules were upregulated during primary infection with both parasite species. Similar to what was observed during O. ostertagi infection, LGALS11 was inducible and strongly upregulated after both primary and repeated infections with C. oncophora. Since LGALS11 was strongly upregulated during primary and repeated O. ostertagi and C. oncophora infections, this galectin was further investigated. LGALS11 induction was associated with the proliferation and de-differentiation of abomasal epithelial cells in culture, independently from the presence of O. ostertagi antigens. In addition, LGALS11 transcript was detected in the abomasal lymph nodes, where it was found in MHCII+ cells; however transcription levels were not altered after primary O. ostertagi infection. In the small intestine, LGALS11 was not only induced by the GI nematode C. oncophora, but also by the protozoan parasite Giardia duodenalis. Although LGALS11 was also transcribed in the lungs, transcription levels were not altered after a natural infection with the lung nematode Dictyocaulus viviparus. These data suggest that LGALS11 induction is rather an undirect effect of the parasite on the epithelium. Upregulation of LGALS11 as a response to parasitic infections is seemingly restricted to the GI tract. A first reason for the different response during O. ostertagi and C. oncophora infection could be related to morphological and physiological differences between the abomasum and the small intestine. A second possible reason are differences in host-parasite interactions such as pathophysiology and immunity. The role of the observed changes during GI nematode infections remains unclear. It was suggested that changes in the mucin barrier during primary infection are not protective since expulsion of O. ostertagi at this stage of the infection is uncommon and levels of mucin-related genes remained unchanged after repeated infections. Galectins on the other hand, especially LGALS1 and LGALS9, could be involved in directing the immune response towards a Th2 response during O. ostertagi infection. LGALS11 could play a role in changing mucus viscosity, regulation of epithelial cell proliferation and differentiation, and immune cell signaling.
Please use this url to cite or link to this publication:
author
promoter
UGent and UGent
organization
year
type
dissertation (monograph)
subject
keyword
mucosal immunity, nematode, gastro-intestinal, mucin, galectin, cattle
pages
188 pages
publisher
Ghent University. Faculty of Veterinary Medicine
place of publication
Merelbeke, Belgium
defense location
Merelbeke : Faculteit Diergeneeskunde (kliniekauditorium B)
defense date
2011-10-11 16:30
ISBN
9789058642714
language
English
UGent publication?
yes
classification
D1
additional info
dissertation consists of copyrighted materials
copyright statement
I have transferred the copyright for this publication to the publisher
id
1937520
handle
http://hdl.handle.net/1854/LU-1937520
date created
2011-10-28 08:21:28
date last changed
2011-10-28 09:23:03
@phdthesis{1937520,
  abstract     = {Gastro-intestinal (GI) nematodes are an important cause of disease and economical loss in livestock industries. The abomasal nematode Ostertagia ostertagi and the intestinal nematode Cooperia oncophora are among the most common parasites infecting cattle in temperate climate regions. In order to develop new therapeutics, a fundamental understanding of the processes involved in protective immunity is needed.
The potential role of mucins and other defensive compounds (trefoil factors/TFF and galectins/LGALS) is described. Nine membrane-bound and six secreted mucins were identified in the bovine genome. The protein architecture of the membrane bound mucins was similar between humans and cattle, while the protein architecture of the gel forming mucins seemed less conserved. The transcriptional distribution of both mucins and mucin glycosyltransferases was investigated in the GI tract of nematode-free cattle. Both sets of genes showed a tissuespecific transcritpion profile and species-specific differences were also observed.
Subsequently, changes in the transcription of mucins, mucin glycosyltransferases and TFFs were investigated in the abomasal mucosa during primary and repeated infections with O. ostertagi. This study showed that the mucin, TFF and glycosyltransferase transcription levels were significantly altered in the abomasal mucosa during primary O. ostertagi infection in cattle. Although the changes in mucin biosynthesis started early after infection, the major effects were observed when adult worms were present at the mucosal surface. In addition, the transcriptional distribution of ten galectins was investigated in the GI tract of uninfected cattle. The majority of the galectins were upregulated at an early time point after infection, before the appearance of adult worms. LGALS1 was also upregulated in repeatedly infected animals, possible indication that it might be involved in the development of protective immunity. LGALS11 was inducibly and strongly upregulated during both primary and repeated infections with O. ostertagi.
The changes in these components in the abomasum during O. ostertagi infections were compared with changes in the small intestine after primary and repeated infections with C. oncophora. The identification of components that are commonly or differentially induced during O. ostertagi and C. oncophora infections might be useful to identify mechanisms involved in protection. For some glycosyltransferases and galectins, differences were observed in the changes in transcription levels. Other molecules were upregulated during primary infection with both parasite species. Similar to what was observed during O. ostertagi infection, LGALS11 was inducible and strongly upregulated after both primary and repeated infections with C. oncophora.
Since LGALS11 was strongly upregulated during primary and repeated O. ostertagi and C. oncophora infections, this galectin was further investigated. LGALS11 induction was associated with the proliferation and de-differentiation of abomasal epithelial cells in culture, independently from the presence of O. ostertagi antigens. In addition, LGALS11 transcript was detected in the abomasal lymph nodes, where it was found in MHCII+ cells; however transcription levels were not altered after primary O. ostertagi infection. In the small intestine, LGALS11 was not only induced by the GI nematode C. oncophora, but also by the protozoan parasite Giardia duodenalis. Although LGALS11 was also transcribed in the lungs, transcription levels were not altered after a natural infection with the lung nematode Dictyocaulus viviparus.
These data suggest that LGALS11 induction is rather an undirect effect of the parasite on the epithelium. Upregulation of LGALS11 as a response to parasitic infections is seemingly restricted to the GI tract.
A first reason for the different response during O. ostertagi and C. oncophora infection could be related to morphological and physiological differences between the abomasum and the small intestine. A second possible reason are differences in host-parasite interactions such as pathophysiology and immunity. The role of the observed changes during GI nematode infections remains unclear. It was suggested that changes in the mucin barrier during primary infection are not protective since expulsion of O. ostertagi at this stage of the infection is uncommon and levels of mucin-related genes remained unchanged after repeated infections.
Galectins on the other hand, especially LGALS1 and LGALS9, could be involved in directing the immune response towards a Th2 response during O. ostertagi infection. LGALS11 could play a role in changing mucus viscosity, regulation of epithelial cell proliferation and differentiation, and immune cell signaling.},
  author       = {Hoorens, Prisca},
  isbn         = {9789058642714},
  keyword      = {mucosal immunity,nematode,gastro-intestinal,mucin,galectin,cattle},
  language     = {eng},
  pages        = {188},
  publisher    = {Ghent University. Faculty of Veterinary Medicine},
  school       = {Ghent University},
  title        = {Mucin and galectin dynamics during gastro-intestinal parasite infections in cattle},
  year         = {2011},
}

Chicago
Hoorens, Prisca. 2011. “Mucin and Galectin Dynamics During Gastro-intestinal Parasite Infections in Cattle”. Merelbeke, Belgium: Ghent University. Faculty of Veterinary Medicine.
APA
Hoorens, P. (2011). Mucin and galectin dynamics during gastro-intestinal parasite infections in cattle. Ghent University. Faculty of Veterinary Medicine, Merelbeke, Belgium.
Vancouver
1.
Hoorens P. Mucin and galectin dynamics during gastro-intestinal parasite infections in cattle. [Merelbeke, Belgium]: Ghent University. Faculty of Veterinary Medicine; 2011.
MLA
Hoorens, Prisca. “Mucin and Galectin Dynamics During Gastro-intestinal Parasite Infections in Cattle.” 2011 : n. pag. Print.