全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

沙眼衣原体pORF5质粒蛋白经TLR2激活MAPKs信号通路诱导人单核细胞产生前炎症细胞因子

DOI: 10.1007/s11427-013-4470-8, PP. 312-318

Keywords: 沙眼衣原体,pORF5质粒蛋白,丝裂原活化蛋白激酶,TLR2,前炎症细胞因子

Full-Text   Cite this paper   Add to My Lib

Abstract:

沙眼衣原体(Chlamydiatrachomatis,Ct)可引起泌尿生殖道感染,导致不孕、异位妊娠等严重并发症.过度的炎症反应被认为是Ct感染造成机体生殖道免疫病理损伤的重要原因,但其具体机制尚不清楚.本研究旨在探讨Ct质粒蛋白pORF5的潜在致炎活性,以及与TLR2和丝裂原活化蛋白激酶(MAPK)信号通路的关系.结果表明,pORF5蛋白以剂量和时间依赖方式诱导THP-1细胞产生TNF-α,IL-1β,IL-8等前炎症细胞因子.进一步研究表明,pORF5蛋白能激活p38/MAPK和ERK/MAPK,但不能激活JNK/MAPK;p38/MAPK和ERK/MAPK特异性抑制剂及TLR2抗体能降低前炎症细胞因子产生水平.该研究初步证实,pORF5质粒蛋白经TLR2活化的p38/MAPK和ERK/MAPK通路诱导THP-1细胞产生前炎症细胞因子,pORF5质粒蛋白可能是Ct重要的致病因子,参与Ct炎症病理过程.

References

[1]  1 Mabey D C, Solomon A W, Foster A. Trachoma. Lancet, 2003, 362: 223-229
[2]  2 Brunham R C, Rey-Ladino J. Immunology of Chlamydia infection: implications for a Chlamydia trachomatis vaccine. Nat Rev Immunol, 2005, 5: 149-161
[3]  3 Belland R, Ojcius D M, Byrne G I. Chlamydia. Nat Rev Microbiol, 2004, 2: 530-531
[4]  4 Cristina Ferreira Silva L, Espinosa Miranda A, Santos Batalha R, et al. Chlamydia trachomatis infection among HIV-infected women attending an AIDS clinic in the city of Manaus, Brazil Braz J Infect Dis, 2012, 16: 335-338
[5]  5 Verteramo R, Pierangeli A, Mancini E, et al. Human papilloma- viruses and genital co-infections in gynaecological outpatients. BMC Infect Dis, 2009, 9: 16-27
[6]  6 Oh J K, Franceschi S, Kim B K, et al. Prevalence of human papillomavirus and Chlamydia trachomatis infection among women attending cervical cancer screening in the Republic of Korea. Eur J Cancer Prev, 2009, 18: 56-61
[7]  7 Buchholz K R, Stephens R S. Activation of the host cell proinflammatory interleukin-8 response by Chlamydia trachomatis. Cell Microbiol, 2006, 8: 1768-1779
[8]  8 Maxion H K, Kelly K A. Chemokine expression patterns differ within anatomically distinct regions of the genital tract during Chlamydia trachomatis infection. Infect Immun, 2002, 70: 1538-1546
[9]  9 Gervassi A, Alderson M R, Suchland R, et al. Differential regulation of inflammatory cytokine secretion by human dendritic cells upon Chlamydia trachomatis infection. Infect Immun, 2004, 72: 7231- 7239
[10]  10 Stephens R S. The cellular paradigm of chlamydial pathogenesis. Trends Microbiol, 2003, 11: 44-51
[11]  11 Thomas N S, Lusher M, Storey C C, et al. Plasmid diversity in Chlamydia. Microbiology, 1997, 143: 1847-1854
[12]  12 O’Connell C M, Ingalls R R, Andrews C W Jr, et al. Plasmid-deficient Chlamydia muridarum fail to induce immune pathology and protect against oviduct disease. J Immunol, 2007, 179: 4027-4034
[13]  13 Li Z, Huang Q, Su S, et al. Localization and characterization of the hypothetical protein CT440 in Chlamydia trachomatis-infected cells. Sci China Life Sci, 2011, 54: 1048-1054
[14]  14 Li Z, Chen C, Chen D, et al. Characterization of fifty putative inclusion membrane proteins encoded in the Chlamydia trachomatis genome. Infect Immun, 2008, 76: 2746-2757
[15]  15 Chen C, Chen D, Sharma J, et al. The hypothetical protein CT813 is localized in the Chlamydia trachomatis inclusion membrane and is immunogenic in women urogenitally infected with C. trachomatis. Infect Immun, 2006, 74: 4826-4840
[16]  16 Zhong G. Chlamydia trachomatis secretion of proteases for manipulating host signaling pathways. Front Microbiol, 2011, 2: 14
[17]  17 Li Z, Chen D, Zhong Y, et al. The chlamydial plasmid-encoded protein pgp3 is secreted into the cytosol of Chlamydia-infected cells. Infect Immun, 2008, 76: 3415-3428
[18]  18 Lei L, Qi M, Budrys N, et al. Localization of Chlamydia trachomatis hypothetical protein CT311 in host cell cytoplasm. Microb Pathog, 2011, 51: 101-109
[19]  19 Greene W, Xiao Y, Huang Y, et al. Chlamydia-infected cells conti- nue to undergo mitosis and resist induction of apoptosis. Infect Immun, 2004, 72: 451-460
[20]  20 Su H, McClarty G, Dong F, et al. Activation of Raf/MEK/ERK/ cPLA2 signaling pathway is essential for chlamydial acquisition of host glycerophospholipids. J Biol Chem, 2004, 279: 9409-9416
[21]  21 Xiao Y, Zhong Y, Greene W, et al. Chlamydia trachomatis infection inhibits both Bax and Bak activation induced by staurosporine. Infect Immun, 2004, 72: 5470-5474
[22]  22 Russell M, Darville T, Chandra-Kuntal K, et al. Infectivity acts as in vivo selection for maintenance of the chlamydial cryptic plasmid. Infect Immun, 2011, 79: 98-107
[23]  23 O’Connell C M, Nicks K M. A plasmid-cured Chlamydia muridarum strain displays altered plaque morphology and reduced infectivity in cell culture. Microbiology, 2006, 152: 1601-1607
[24]  24 Carlson J H, Whitmire W M, Crane D D, et al. The Chlamydia trachomatis plasmid is a transcriptional regulator of chromosomal genes and a virulence factor. Infect Immun, 2008, 76: 2273-2283
[25]  25 Srivastava P, Vardhan H, Bhengraj A R, et al. Azithromycin treatment modulates the extracellular signal-regulated kinase mediated pathway and inhibits inflammatory cytokines and chemokines in epithelial cells from infertile women with recurrent Chlamydia trachomatis infection. DNA Cell Biol, 2011, 30: 545-554
[26]  26 Vignola M J, Kashatus D F, Taylor G A, et al. cPLA2 regulates the expression of type I interferons and intracellular immunity to Chlamydia trachomatis. J Biol Chem, 2010, 285: 21625-21635
[27]  27 Darville T, O’Neill J M, Andrews C W Jr, et al. Toll-like receptor-2, but not Toll-like receptor-4, is essential for development of oviduct pathology in chlamydial genital tract infection. J Immunol, 2003, 171: 6187-6197
[28]  28 He X, Nair A, Mekasha S, et al. Enhanced virulence of Chlamydia muridarum respiratory infections in the absence of TLR2 activation. PLoS ONE, 2011; 6: e20846
[29]  29 O’Connell C M, AbdelRahman Y M, Green E, et al. Toll-like receptor 2 activation by Chlamydia trachomatis is plasmid dependent, and plasmid-responsive chromosomal loci are coordinately regulated in response to glucose limitation by C. trachomatis but not by C. muridarum. Infect Immun, 2011, 79: 1044-1056

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133