期刊论文详细信息
BMC Infectious Diseases
Proteomic analysis of extremely severe hand, foot and mouth disease infected by enterovirus 71
Li Zhu3  Jian-Ping Tao1  Jun-Hong Lin1  Gen-Quan Yin1  Chun-Hui He1  Li-Jia Mao1  Yu-Fen Xu1  Chao-Wu Liu4  Hong-Ling Jia2  Li Deng1 
[1] Guangzhou Women and Children′s medical center, Guangzhou 510120, Guangdong, China;Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, 510632, China;School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou 510515, Guangdong, China;Guangdong Institute of Microbiology/Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangzhou 510070, Guangdong, China
关键词: Proteomic analysis;    MALDI-TOF/TOF MS;    Extremely severe HFMD;   
Others  :  1146081
DOI  :  10.1186/1471-2334-13-383
 received in 2013-03-10, accepted in 2013-08-16,  发布年份 2013
PDF
【 摘 要 】

Background

To clarify the molecular mechanisms that participate in the severe hand, foot and mouth disease (HFMD) infected by Enterovirus 71 and to detect any related protein biomarkers, we performed proteomic analysis of protein extracts from 5 extremely severe HFMD children and 5 healthy children.

Methods

The protein profiles of them were compared using two-dimensional electrophoresis. Differentially expressed proteins were identified using mass spectrometry. Functional classifications of these proteins were based on the PANTHER. The interaction network of the differentially expressed protein was generated with Pathway Studio.

Results

A total of 38 differentially expressed proteins were identified. Functional classifications of these proteins indicated a series of altered cellular processes as a consequence of the severe HFMD. These results provided not only new insights into the pathogenesis of severe HFMD, but also implications of potential therapeutic designs.

Conclusions

Our results suggested the possible pathways that could be the potential targets for novel therapy: viral protection, complement system and peroxide elimination.

【 授权许可】

   
2013 Deng et al.; licensee BioMed Central Ltd.

【 预 览 】
附件列表
Files Size Format View
20150403090952197.pdf 2985KB PDF download
Figure 4. 106KB Image download
Figure 3. 63KB Image download
Figure 2. 99KB Image download
Figure 1. 76KB Image download
【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

【 参考文献 】
  • [1]Schmidt NJ, Lennette EH, Ho HH: An apparently new enterovirus isolated from patients with disease of the central nervous system. J Infect Dis 1974, 129(3):304-309.
  • [2]Lum LC, Wong KT, Lam SK, Chua KB, Goh AY, Lim WL, Ong BB, Paul G, AbuBakar S, Lambert M: Fatal enterovirus 71 encephalomyelitis. J Pediatr 1998, 133(6):795-798.
  • [3]Lum LC, Wong KT, Lam SK, Chua KB, Goh AY: Neurogenic pulmonary oedema and enterovirus 71 encephalomyelitis. Lancet 1998, 352(9137):1391.
  • [4]Ho M, Chen ER, Hsu KH, Twu SJ, Chen KT, Tsai SF, Wang JR, Shih SR: An epidemic of enterovirus 71 infection in Taiwan. Taiwan Enterovirus Epidemic Working Group. N Engl J Med 1999, 341(13):929-935.
  • [5]Chan KP, Goh KT, Chong CY, Teo ES, Lau G, Ling AE: Epidemic hand, foot and mouth disease caused by human enterovirus 71, Singapore. Emerg Infect Dis 2003, 9(1):78-85.
  • [6]Zhang Y, Tan XJ, Wang HY, Yan DM, Zhu SL, Wang DY, Ji F, Wang XJ, Gao YJ, Chen L, et al.: An outbreak of hand, foot, and mouth disease associated with subgenotype C4 of human enterovirus 71 in Shandong. China. J Clin Virol 2009, 44(4):262-267.
  • [7]Zhang Y, Zhu Z, Yang W, Ren J, Tan X, Wang Y, Mao N, Xu S, Zhu S, Cui A: An emerging recombinant human enterovirus 71 responsible for the 2008 outbreak of hand foot and mouth disease in Fuyang city of China. Virol J 2008, 7:94.
  • [8]Jia L, Zhao CS, Zhang L, Li S, Zhang DT, Liu BW, Wang QY, Li XY: [Comparisons of epidemiological and clinical characteristics in children with hand-foot-mouth disease caused by Enterovirus 71 and Coxackievirus A16]. Zhongguo Dang Dai Er Ke Za Zhi 2011, 13(8):635-637.
  • [9]Wang X, Zhu C, Bao W, Zhao K, Niu J, Yu XF, Zhang W: Characterization of full-length enterovirus 71 strains from severe and mild disease patients in northeastern China. PLoS One 2012, 7(3):e32405.
  • [10]Wang SM, Liu CC: Enterovirus 71: epidemiology, pathogenesis and management. Expert Rev Anti Infect Ther 2009, 7(6):735-742.
  • [11]Chen SC, Chang HL, Yan TR, Cheng YT, Chen KT: An eight-year study of epidemiologic features of enterovirus 71 infection in Taiwan. Am J Trop Med Hyg 2007, 77(1):188-191.
  • [12]Briese T, Palacios G, Kokoris M, Jabado O, Liu Z, Renwick N, Kapoor V, Casas I, Pozo F, Limberger R, et al.: Diagnostic system for rapid and sensitive differential detection of pathogens. Emerg Infect Dis 2005, 11(2):310-313.
  • [13]Foo DG, Ang RX, Alonso S, Chow VT, Quak SH, Poh CL: Identification of immunodominant VP1 linear epitope of enterovirus 71 (EV71) using synthetic peptides for detecting human anti-EV71 IgG antibodies in Western blots. Clin Microbiol Infect 2008, 14(3):286-288.
  • [14]Wang SY, Lin TL, Chen HY, Lin TS: Early and rapid detection of enterovirus 71 infection by an IgM-capture ELISA. J Virol Methods 2004, 119(1):37-43.
  • [15]Xu F, Yan Q, Wang H, Niu J, Li L, Zhu F, He S, Zhang S, Weng Z, Cheng T: Performance of detecting IgM antibodies against enterovirus 71 for early diagnosis. PLoS One 2010, 5(6):e11388.
  • [16]Sherman M, Peltekian KM, Lee C: Screening for hepatocellular carcinoma in chronic carriers of hepatitis B virus: incidence and prevalence of hepatocellular carcinoma in a North American urban population. Hepatology 1995, 22(2):432-438.
  • [17]Jia H, Liu C, Ge F, Xiao C, Lu C, Wang T, He Q: Identification of ubiquitinated proteins from human multiple myeloma U266 cells by proteomics. Biomed Environ Sci 2011, 24(4):422-430.
  • [18]Xiao CL, Zhang ZP, Xiong S, Lu CH, Wei HP, Zeng HL, Liu Z, Zhang XE, Ge F: Comparative proteomic analysis to discover potential therapeutic targets in human multiple myeloma. Proteomics Clin Appl 2009, 3(11):1348-1360.
  • [19]Deng L, Jia HL, Liu CW, Hu KH, Yin GQ, Ye JW, He CH, Chen JH, Xie YP, Dang R: Analysis of differentially expressed proteins involved in hand, foot and mouth disease and normal sera. Clin Microbiol Infect 2012, 18(6):E188-196.
  • [20]Enghild JJ, Salvesen G, Thogersen IB, Valnickova Z, Pizzo SV, Hefta SA: Presence of the protein-glycosaminoglycan-protein covalent cross-link in the inter-alpha-inhibitor-related proteinase inhibitor heavy chain 2/bikunin. J Biol Chem 1993, 268(12):8711-8716.
  • [21]Sunthornthepvarakul T, Angkeow P, Weiss RE, Hayashi Y, Refetoff S: An identical missense mutation in the albumin gene results in familial dysalbuminemic hyperthyroxinemia in 8 unrelated families. Biochem Biophys Res Commun 1994, 202(2):781-787.
  • [22]Ichinose A, Espling ES, Takamatsu J, Saito H, Shinmyozu K, Maruyama I, Petersen TE, Davie EW: Two types of abnormal genes for plasminogen in families with a predisposition for thrombosis. Proc Natl Acad Sci U S A 1991, 88(1):115-119.
  • [23]Sjoberg AP, Trouw LA, Blom AM: Complement activation and inhibition: a delicate balance. Trends Immunol 2009, 30(2):83-90.
  • [24]Ricklin D, Hajishengallis G, Yang K, Lambris JD: Complement: a key system for immune surveillance and homeostasis. Nat Immunol 2010, 11(9):785-797.
  • [25]Zhang C, Xu Y, Jia L, Yang Y, Wang Y, Sun Y, Huang L, Qiao F, Tomlinson S, Liu X: A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitor. Virol J 2010, 7:30. BioMed Central Full Text
  • [26]Shih SR, Stollar V, Lin JY, Chang SC, Chen GW, Li ML: Identification of genes involved in the host response to enterovirus 71 infection. J Neurovirol 2004, 10(5):293-304.
  • [27]Crack PJ, Taylor JM, Flentjar NJ, De Haan J, Hertzog P, Iannello RC, Kola I: Increased infarct size and exacerbated apoptosis in the glutathione peroxidase-1 (Gpx-1) knockout mouse brain in response to ischemia/reperfusion injury. J Neurochem 2001, 78(6):1389-1399.
  • [28]Hussain SP, Amstad P, He P, Robles A, Lupold S, Kaneko I, Ichimiya M, Sengupta S, Mechanic L, Okamura S, et al.: p53-induced up-regulation of MnSOD and GPx but not catalase increases oxidative stress and apoptosis. Cancer Res 2004, 64(7):2350-2356.
  • [29]Kuku I, Aydogdu I, Bayraktar N, Kaya E, Akyol O, Erkurt MA: Oxidant/antioxidant parameters and their relationship with medical treatment in multiple myeloma. Cell Biochem Funct 2005, 23(1):47-50.
  文献评价指标  
  下载次数:64次 浏览次数:9次