The influence of porcine epidemic diarrhea virus on pig small intestine mucosal epithelial cell function
- 189 Downloads
Porcine epidemic diarrhea (PED) is a highly contagious, acute enteric tract infectious disease of pigs (Sus domesticus) caused by porcine epidemic diarrhea virus (PEDV). PED is characterized by watery diarrhea, dehydration, weight loss, vomiting and death. PEDV damages pig intestinal epithelial tissue, causing intestinal hyperemia and atrophy of intestinal villi, with formation of intestinal epithelial cell cytoplasmic vacuoles. Since pig small intestinal epithelial cells (IECs) are target cells of PEDV infection, IEC cells were utilized as a model for studying changes in cellular activities post-PEDV infection. Monitoring of Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities demonstrated that PEDV infection decreased these activities. In addition, IECs proliferation was shown to decrease after PEDV infection using an MTT assay. Moreover, IECs apoptosis detected by flow cytometry with propidium iodide (PI) staining was clearly shown to increase relative to the control group. Meanwhile, animal experiments indicated that PEDV virulence for IEC cells was greater than viral virulence for Vero cells, although this may be due to viral attenuation after numerous passages in the latter cell line. Collectively, these studies revealed viral pathogenic mechanisms in PEDV-infected IECs and offer a theoretical basis for PEDV prevention and control.
XW designed the experiment. XW, TZ and CJ completed the experiment and analyzed the data. The manuscript was written using contributions of all authors and all authors have given approval to the final version of the manuscript.
This work was supported by the National Natural Science Foundation of China (Grant #: 31072115).
Compliance with ethical standards
Conflicts of interest
The authors declare that there are no conflicts of interest in this paper.
Animal experimentation was conducted strictly according to the recommendations of the Guide for the Care and Use of Laboratory Animals of the Ministry of Health, China. Our protocol was reviewed and approved by the Research Ethics Committee of Northwest A&F University.
- 4.Kim YK, Lim SI, Cho IS, Cheong KM, Lee EJ, Lee SO, Kim JB, Kim JH, Jeong DS, An BH, An DJ (2015) A novel diagnostic approach to detecting porcine epidemic diarrhea virus: the lateral immunochromatography assay. J Virol Methods 225:4–8. https://doi.org/10.1016/j.jviromet.2015.08.024 CrossRefGoogle Scholar
- 10.Hofmann M, Wyler R (1988) Propagation of the virus of porcine epidemic diarrhea in cell culture. J Clin Microbiol 26:2235–2239Google Scholar
- 13.Pavlov KV, Sokolov VS (2000) Electrogenic ion transport by Na+, K+-ATPases. Membr Cell Bio 13:745–788Google Scholar
- 15.Norouzi-Javidan A, Javanbakht J, Barati F, Fakhraei N, Mohammadi F, Dehpour AR (2015) Serotonin 5-HT7 receptor agonist, LP-211, exacerbates Na(+), K(+)-ATPase/Mg(2+)-ATPase imbalances in spinal cord-injured male rats. Diagn Pathol 10:157. https://doi.org/10.1186/s13000-015-0397-7 CrossRefGoogle Scholar
- 18.Rose AM, Valdes R Jr (1994) Understanding the sodium pump and its relevance to disease. Clin Chem 40:1674–1685Google Scholar
- 19.Shah S, Kongre V, Kumar V, Bharadwaj R (2016) A study of parasitic and bacterial pathogens associated with diarrhea in HIV-positive patients. Cureus 8:e807Google Scholar
- 20.Zhao J, Shi BJ, Huang XG, Peng MY, Zhang XM, He DN, Pang R, Zhou B, Chen PY (2013) A multiplex RT-PR assay for rapid and differential diagnosis of four porcine diarrhea associated viruses in field samples from pig farms in East China from 2010 to 2012. J Virol Methods 194:107–112. https://doi.org/10.1016/j.jviromet.2013.08.008 CrossRefGoogle Scholar
- 21.Reed LJ, Muench H (1938) A simple method of estimating fifty per cent endpoints. Am J Hyg 27:493–497Google Scholar
- 23.Manoharan P, Gayam S, Arthur S, Palaniappan B, Singh S, Dick GM, Sundaram U (2015) Chronic and selective inhibition of basolateral membrane Na-K-ATPase uniquely regulates brush border membrane Na absorption in intestinal epithelial cells. Am J Physiol Cell Physiol 308:C650–C656. https://doi.org/10.1152/ajpcell.00355.2014 CrossRefGoogle Scholar
- 26.Ziegelhoffer A, Kjeldsen K, Bundgaard H, Breier A, Vrbjar N, Dzurba A (2000) Na, K-ATPase in the myocardium: molecular principles, functional and clinical aspects. Gen Physiol Biophys 19:9–47Google Scholar