Abstract
Infections in cattle with the gastric nematode Ostertagia ostertagi are associated with decreased acid secretion and profound physio-morphological changes of the gastric mucosa. The purpose of the current study was to investigate the mechanisms triggering these pathophysiological changes. O. ostertagi infection resulted in a marked cellular hyperplasia, which can be explained by increased transcriptional levels of signaling molecules related to the homeostasis of gastric epithelial cells such as HES1, WNT5A, FGF10, HB-EGF, AREG, ADAM10 and ADAM17. Intriguingly, histological analysis indicated that the rapid rise in the gastric pH, observed following the emergence of adult worms, cannot be explained by a loss of parietal cells, as a decrease in the number of parietal cells was only observed following a long term infection of several weeks, but is likely to be caused by an inhibition of parietal cell activity. To investigate whether this inhibition is caused by a direct effect of the parasites, parietal cells were co-cultured with parasite Excretory/Secretory products (ESP) and subsequently analyzed for acid production. The results indicate that adult ESP inhibited acid secretion, whereas ESP from the L4 larval stages did not alter parietal cell function. In addition, our data show that the inhibition of parietal cell activity could be mediated by a marked upregulation of inflammatory factors, which are partly induced by adult ESP in abomasal epithelial cells. In conclusion, this study shows that the emergence of adult O. ostertagi worms is associated with marked cellular changes that can be partly triggered by the worm’s Excretory/secretory antigens.
Highlights
Infections with the abomasal nematode Ostertagia ostertagi are considered as a major source of economic losses in cattle throughout the temperate regions of the world
It has been shown that these mucosal changes can be triggered by a local inflammatory response, as increased expression levels of pro-inflammatory factors such as IL1B, TNFA and prostaglandin E2 (PGE2) are associated with the impairment of parietal cell function and the alterations of mucosal cell homeostasis [13,14,15,16]
Impact of O. ostertagi infection on mucosal cell proliferation In order to determine the impact of an O. ostertagi infection on mucosal cell proliferation, tissue sections were stained for Ki-67 as a cell proliferation marker (Figure 1)
Summary
Infections with the abomasal nematode Ostertagia ostertagi are considered as a major source of economic losses in cattle throughout the temperate regions of the world. O. ostertagi infection results in profound physio-morphological and functional alterations of gastric mucosal cells [1]. The gastric fundic mucosa is organized in well-defined units referred to as gastric glands composed by different cell lineages [2]. Homeostasis of this highly renewing epithelium is under a tight regulation of different molecular and cellular signaling pathways that keep a balance between proliferation and differentiation of the different gastric cell populations. In addition to inflammatory factors, changes in expression levels of SHH (Sonic Hedgehog), FGF (Fibroblast Growth Factors), BMP (Bone Morphogenetic proteins), WNT (WinglessType) and NOTCH could induce an imbalance between cell proliferation and cell differentiation in the gastric mucosa [3]. The role played by all these factors in the pathogenesis of abomasal ostertagiosis is still unknown
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