Gene Expression Profile in the Liver of Sheep Infected with Cystic Echinococcosis

Abstract

BackgroundCystic Echinococcosis (CE), caused by infection with the Echinococcus granulosus (E. granulosus), represents considerable health problems in both humans and livestock. Nevertheless, the genetic program that regulates the host response to E. granulosus infection is largely unknown. Previously, using microarray analysis, we found that the innate immunity played a vital role in the E. granulosus defense of the intestine tissue where E. granulosus first invaded. Subsequently, we turned our attention to investigating the molecular immune mechanism in its organ target, the liver, which is where the E. granulosus metacestodes are established and live for very long periods. In this work, the microarray-based methodology was used to study gene expression profiles in the liver of sheep infected with E. granulosus at 8 weeks post infection, corresponding to the early cystic established phase.MethodsA total of 6 female-1-year-old healthy Kazakh sheep were used for the experiments. Three Kazakh sheep were orally infected with E. granulosus eggs, and the others remained untreated and served as controls. Sheep were humanely euthanized and necropsized at 8 weeks post-infection (the early stage of cyst established). The microarray was used to detect differential hepatic gene expression between CE infection sheep and healthy controls at this time point. Real-time PCR was used to validate the microarray data.ResultsWe found that E. granulosus infection induces 153 differentially expressed genes in the livers of infected sheep compared with healthy controls. Among them, 87 genes were up-regulated, and 66 genes were notably down-regulated. Functional analysis showed that these genes were associated with three major functional categories: (a) metabolism, (b) the immune system and (c) signaling and transport. Deeper analysis indicated that complement together with other genes associated with metabolism, played important roles in the defense of E. granulosus infection.ConclusionThe present study identified genes profiling in the liver tissue of E. granulosus infection in sheep. The expression pattern obtained here could be helpful for understanding the molecular immunity mechanisms of host responses to E. granulosus infection. However, it is necessary to carry out further studies to evalute the role of these genes.

Proteomics investigation of human sera for determination of postoperative indicators of pulmonary cystic echinococcosis

“…Among them a total of ten protein spots have been selected for identification with mass spectrometry including: APOA1, BGN, SPP2, EAF1 ACOXL, MRPL55, MCTP2, SEPTIN1, B4GALNT1, and ZNF843. Some of these proteins have been reported earlier from hydatid fluid in sheep liver CE [ 54 ]. However, they have not been reported from human sera of CE patients, so far.…”

Insights into the genomic homogeneity of Moroccan indigenous sheep breeds though the lens of runs of homozygosity

“…ATP5PF is known for its involvement in energy metabolism 50 , GABPA has been related to milk production traits 51 , JAM2 has been implicated in immunity to gastrointestinal parasites 52 , and MRPL39 is associated with mitochondrial function and aerobic metabolism 53 . This compilation of genes within ROH islands underscores their potential importance in the adaptation and physiological characteristics of these sheep breeds.…”

Identification of candidate biomarkers of liver hydatid disease via microarray profiling, bioinformatics analysis, and machine learning

“… 19 Gene expression profiling in the liver of Echinococcus -infected sheep showed 87 upregulated genes and 66 downregulated genes, which were correlated with signaling and transport, the immune system, and metabolism. 20 Transcriptional profiling reveals that cytokine/chemokine factors are involved in the infection of Echinococcus multilocularis in mice. 21 The gene expression profile in the liver of Echinococcus -infected mice indicates that chemokine-activated MAPK signaling and the peroxisome proliferator-induced PPAR (peroxisome proliferator-activated receptor) pathway respond to the infection in the system.…”