| Campylobacter jejuni is among the leading bacterial causes of human gastroenteritis worldwide, about90%of acute gastroenteritis associates with C. jejuni in clinical. In Europe and the US, the morbidity has been more than Salmonella, Shigella, and Escherichia coli O157:H7. In addition to cause enteritis, C. jejuni is one of the main factors for GBS. It is reported that the risk of developing GBS during the2months following a symptomatic episode of C.jejuni infection is approximately100times higher than the risk in the general population. The GBS, also known as acute inflammatory demyelinating polyneuropathy (AIDP), is an autoimmune peripheral neuropathy disorder mediated by body fluids and cells. Serious disease can be fatal with the mortality rate of5%～10%. Due to its high rate of infection and subsequent potential threats, C. jejuni has received close attention.The main purposes of this study are:(1) using Bama miniature pigs to established animal model which C. jejuni induced GBS;(2) trying to find pathogenesis-related genes in the GBS model animal and understand their function.1Establishment of an animal model for C. jejuni induced GBSC. jejuni which can lead to people suffering from GBS was selected to infect pigs. Four groups, each of four, were oral-infused bacterial suspension with3×1012cfu/ml,3×1011cfu/ml,3×1010cfu/ml,3×109cfu/ml in four concentrations. A control group which was oral-infused normal saline was also set up. From the second week, tissue samples and blood samples were collected regularly to determine the lesions by ELISA and biopsy. There were12of the total16samples in pathological group were positive with GM1-IgG antibodies, positive rate was81.25%. However, there was no significant difference between the gradient. The results of H/E staining showed neuronophagia, enlarged Virchow-Robin spaces, central chromatolysis, and so on in the cerebrum of the onset animals; LFB staining showed mildly demyeliantion in the cerebellar white matter and the lumbar enlargement of the onset animals. The result showed that the drug concentration of the best attack was3×109cfu/ml～3×1012 cfu/ml and the best time to collect blood and tissue samples was4-5weeks after inoculation.2Gene expression profile of C.jejuni induced GBS in Bama miniature pigsBased on the results of the pathological tissue sections and immunological test, we selected the typical diseased tissue and control. By using porcine whole genome microarray purchased from Affymetrix, we found2156differentially expressed probes,896of which were up-regulated, while the others were down-regulated (P<0.05,FDR <0.05). These probes were related to222genes,114of which were up-regulated while108were down-regulated. Based on Gene Ontology database, all of the222differences genes were annotated, we obtained130significant GOs (P<0.05, FDR <0.05), of which there were55related to up-regulated genes, and75related to down-regulated gene. Basing on the KEGG database, we analyzed the signal transduction pathways in which all of the differential genes were involved.127Pathways were found related with the222differential genes. Fisher’s exact test and chi-square tests were used to analyze the significance, we got30significance Pathways of the up-regulated genes and37significance Pathways of the down-regulated genes (P<0.05). Construct the lesion and control co-expression networks using the genes within the intersection which come from significant genes from the GO and Pathway. We found21key genes, in which HPRT1, PKC and PPARGC-1took up core sites in the network,11genes including PPARGC-1, SUS2DD, and AMPKA2were suppressed in sick animals. |
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