Analysis of cell hyperplasia and parietal cell dysfunction induced by Ostertagia ostertagi infection

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.

Abnormal amphiregulin expression correlates with gastric cancer prognosis

“…As a pro-oncogenic molecule, aberrant expression of AREG could promote abnormal activation of cell signaling transduction and subsequent gene transcription, which, in turn, could lead to cancer development and progression [22–24]. As an ectodomain of transmembrane glycoprotein of precursor, AREG is over-expressed in the epithelial tissue of gastric [25], pancreatic [26], colon, and prostate cancer [27], as well as renal cell carcinoma [28]. After proteolytic cleavage, the shedding ectodomain of pro-AREG is secreted into the blood and other body fluids as a soluble growth factor [8].…”

Hitting an Unintended Target: Phylogeography of Bombus brasiliensis Lepeletier, 1836 and the First New Brazilian Bumblebee Species in a Century (Hymenoptera: Apidae)

“…It could be argued that the phylogenetic hypothesis produced here, being based on two linked genes (maternally-inherited mtDNA), may merely indicate a phylogeny for those genes, which may be different from the correct phylogeny of the species involved (for example [ 48 ]). Nevertheless, as pointed out by Williams et al [ 49 ], this problem has not been detected for the use of COI in bumblebees and, moreover, mt DNA may actually be more suitable for species delimitation than other molecular and morphological data [ 50 ].…”

“…Bombus is a relatively monotonous genus, as far as morphological characters are concerned (for example [ 1 ]), and this makes them frequently difficult to distinguish, especially among closely-related species (for example [ 5 – 11 , 49 ]. Thus, it is not surprising that not a single exclusive autoapomorphy of B .…”

“…Local or regional decline or extirpation of bumblebee populations has been reported in the northern hemisphere (for example [ 49 , 67 – 70 ]) and in Brazil [ 71 ]. It seems that the small available sample of B .…”

Prevalence of Ostertagia ostertagi lesions in slaughtered dairy cattle from São Miguel Island, Azores, Portugal

“…With all the alterations in the abomasum mucosa (i.e. gastric mucosa hiperplasia, decrease of parietal and peptic cells), adult animals with ostertagiosis, can suffer at long term, due to diminished nutrient absorption (Taylor et al, 2007;Rinaldi et al, 2011;Mihi et al, 2013;. Besides the weight loss and decreased weight gain and carcass quality, other factors need to be included to the economic impact such as: feeding expenses to compensate weight loss; delay in reaching reproductive weight and inherent production losses (reproductive and milk production losses); decreased milk production and decreased reproductive performance (increased calving-to-conception interval) (Charlier et al, 2009;McElroy & de Buron, 2014;Knapp-Lawitzke et al, 2015).…”