Advance on the effects of lipopolysaccharide receptor complex on iris pigment epithelial cells in acute anterior uveitis

doi:10.3877/cma.j.issn.2095-2007.2023.03.008

Abstract

Abstract:

Recently, it has been demonstrated that iris pigment epithelial cells of human uveal have had inherent pattern recognition receptors for the lipopolysaccharide response (LPS), such as Toll-like receptor (TLR)4, myeloid differential protein (MD)-2 and cluster of differentiation (CD)14, which expanding the current understanding of microbial triggers and uveal innate immune in the pathogenesis of acute anterior uveitis. The result point out components of the LPS receptor complex may serve as effective targets for the treatment. The research status of LPS receptor complex in human iris pigment epithelial cells and uveitis in animal models were reviewed.

Key words: Acute anterior uveitis, Iris pigment epithelial cells, Lipopolysaccharide receptor complex

Ziwei Zhang, Hong Lu. Advance on the effects of lipopolysaccharide receptor complex on iris pigment epithelial cells in acute anterior uveitis[J]. Chinese Journal of Ophthalmologic Medicine(Electronic Edition), 2023, 13(03): 167-171.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhykyxzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-2007.2023.03.008

https://zhykyxzz.cma-cmc.com.cn/EN/Y2023/V13/I03/167

Figures/Tables 1

References 56

[21]	Tsukamoto H, Takeuchi S, Kubota K, et al. Lipopolysaccharide (LPS)－binding protein stimulates CD14－dependent Toll－like receptor 4 internalization and LPS－induced TBK1－IKK－IRF3 axis activation[J]. J Biol Chem, 2018, 293(26): 10186－10201.
[22]	李永旺，麻莉，张德明，等. 抗LBP多抗对LPS诱导的肺组织NF－κB活化的抑制作用[J]. 解放军医学杂志，2003，28(2)：125－127.
[23]	吴学玲，赵云峰，徐德斌，等. LBP抑制肽对LPS诱导的小鼠内毒素血症肺组织NF－κB活性的影响[J]. 现代免疫学，2009，29(2)：45－49.
[24]	Liu A, Weiss S, Fang H, et al. Lipopolysaccharide－binding protein (LBP) blockade augments the protective effect of granulo－cyte colony－stimulating factor (G－CSF) in a rat sepsis model[J]. Shock, 2015, 43(5): 497－503.
[25]	Póciennikowska A, Hromada－Judycka A, Borzcka K, et al. Co－operation of TLR4 and raft proteins in LPS－induced pro－inflammatory signaling[J]. Cell Mol Life Sci, 2015, 72(3): 557－581.
[26]	Correia JDS, Soldau K, Christen U, et al. Lipopolysaccharide is in close proximity to each of the proteins in its membrane receptor complex transfer from CD14 To TLR4 And MD－2[J]. J Biol Chem, 2001, 276(24): 21129－21135.
[27]	Ryu JK, Kim SJ, Rah SH, et al. Reconstruction of LPS transfer cascade reveals structural determinants within LBP, CD14, and TLR4－MD2 for efficient LPS recognition and transfer[J]. Immunity, 2016, 46(1): 38－50.
[28]	Kim JI, Lee CJ, Jin MS, et al. Crystal structure of CD14 and its implications for lipopolysaccharide signaling[J]. J Biol Chem, 2005, 280(12): 11347－11351.
[29]	Chui J, Li M, Di GN, et al. Iris pigment epithelial cells express a functional lipopolysaccharide receptor complex[J]. Invest Ophthalmol Vis, 2010, 51(5): 2558－2567.
[30]	李上，卢弘，胡小凤，等. TLR4－MyD88在大鼠急性前葡萄膜炎虹膜中的表达[J]．中华实验眼科杂志，2010，28(2)：97－102.
[31]	Brito BE, Zamora DO, Bonnah RA, et al. Toll－like receptor 4 and CD14 expression in human ciliary body and TLR－4 in human iris endothelial cells[J]. Exp Eye Res, 2004, 79(2): 203－208.
[32]	Elner SG, Petty HR, Elner VM, et al. TLR4 mediates human retinal pigment epithelial endotoxin binding and cytokine expression[J]. Invest Ophthalmol Vis, 2005, 46(12): 4627－4633.
[33]	Elner VM, Elner SG, Zong MB, et al. RPE CD14 immunohistochemical, genetic, and functional expression[J]. Exp Eye Res, 2003, 76(3): 321－331.
[34]	Liu S, Khemlani LS, Shapiro RA, et al. Expression of CD14 by hepatocytes: upregulation by cytokines during endotoxemia[J]. Infect Immun Pharmacol, 1998, 66(11): 5089－5098.
[35]	Kim HM, Park BS, Kim JI, et al. Crystal structure of the TLR4－MD－2 complex with bound endotoxin antagonist Eritoran[J]. Cell, 2007, 130(5): 906－917.
[36]	Raetz CRH, Reynolds CM, Trent MS, et al. Lipid A modifica－tion systems in gram－negative bacteria[J]．Annu Rev Biochem, 2007, 76(1): 295－329.
[37]	Park B, Brinkmann MM, Spooner E, et al. Proteolytic cleavage in an endolysosomal compartment is required for activation of Toll－like receptor 9[J]. Nat Immunol, 2008, 9(12): 1407－1414.
[38]	Zhang Y, Wu J, Ying S, et al. Discovery of new MD2 inhibitor from chalcone derivatives with anti－inflammatory effects in LPS－induced acute lung injury[J]. Sci Rep, 2016, 6: e25130.
[39]	Fang Q, Wang J, Zhang Y, et al. Inhibition of myeloid differentiation factor－2 attenuates obesity－induced cardiomyopathy and fibrosis[J]. BiochimBiophys Acta Mol Basis Dis, 2018, 1864(1): 252－262.
[40]	Chen X, Yu W, Li W, et al. An anti－inflammatory chalcone derivative prevents heart and kidney from hyperlipidemia－induced injuries by attenuating inflammation[J]. Toxicol Appl Pharmacol, 2018, 338: 43－53.
[41]	Han J, Zou C, Mei L, et al. MD2 mediates angiotensin II－induced cardiac inflammation and remodeling via directly binding to Ang II and activating TLR4/NFκB signaling pathway[J]. Basic Res Cardiol, 2017, PMID: 28013347.
[42]	段光杰. 内毒素拮抗肽抑制脂多糖诱导的过度炎症反应及其机制研究[D]．重庆：第三军医大学，2010.
[43]	Zanoni I, Ostuni R, Marek LR, et al. CD14 controls the LPS－induced endocytosis of Toll－like receptor 4[J]. Cell, 2011, 147(4): 868－880.
[44]	Rocha DM, Caldas AP, Oliveira LL, et al. Saturated fatty acids trigger TLR4－mediated inflammatory response[J]. Atherosclero－sis, 2016, 244: 211－215.
[45]	Suzuki Y, Ohgami K, Shiratori K, et al. Suppressive effects of astaxanthin against rat endotoxin－induced uveitis by inhibiting the NF－κB signaling pathway[J]. Exp Eye Res, 2006, 82(2): 275－281.
[46]	Todaro M, Zerilli M, Triolo G, et al. NFκB protects Behet′s disease T cells against CD95－induced apoptosis up－regulating antiapoptotic proteins[J]. Arthritis Rheum, 2005, 52(7): 2179－2191.
[47]	Li S, Lu H, Hu X, et al. Expression of TLR4－MyD88 and NFκB in the Iris during Endotoxin－Induced Uveitis[J]. Mediators Inflamm, 2010, PMID: 20847811.
[48]	Wang J, Lu H, Hu X, et al. Nuclear factor translocation and acute anterior uveitis[J]. Mol Vis, 2011, 17(21): 170－176.
[49]	许邦丽，王婧，齐欣，等. 内毒素诱导的葡萄膜炎中虹膜固有组织细胞上MyD88与TLR－4的共表达[J]. 眼科新进展，2012，32(4)：4.
[50]	Kezic J, Taylor S, Gupta S, et al. Endotoxin－induced uveitis is primarily dependent on radiation－resistant cells and on MyD88 but not TRIF[J]. J Leukoc Biol, 2011, 90(2): 305－311.
[51]	王婧，刘新丽，吴慧茹，等. 红芪多糖干预内毒素诱导的大鼠葡萄膜炎的机制[J]. 眼科新进展，2019，39(7)：606－610.
[52]	Hubbard L, Moore BB. IRAK－M regulation and function in host defense and immune homeostasis[J]. Infect Dis Rep, 2010, 2(1): e9.
[53]	Seki M, Kohno S, Newstead MW, et al. Critical role of IL－1 receptor－associated kinase－M in regulating chemokine－dependent deleterious inflammation in murine influenza pneumonia[J]. J Immunol, 2010, 184(3): 1410－1418.
[1]	Rosenbaum JT, McDevitt HO, Guss RB, et al. Endotoxin－induced uveitis in rats as a model for human disease[J]. Nature, 1980, 286(5773): 611－613.
[2]	杨培增. 内毒素诱导大鼠葡萄膜炎的组织平片和切片研究[J]. 中华眼底病杂志，1996，12(1)：4.
[3]	马翠萍，金浩丽，杨培增，等. 伤寒杆菌内毒素诱导的SD大鼠全葡萄膜炎[J]. 中山大学学报，2001，22(6)：451－453.
[4]	卢弘. 霍乱弧菌内毒素诱导大鼠葡萄膜炎的组织切片研究[J]. 眼科新进展，2002, 22(6)：384－386.
[5]	Del－Fresno C, Garcia－Rio F, Gomez－Pina V, et al. Potent phagocytic activity with impaired antigen presentation identifying lipopolysaccharide－tolerant human monocytes: demonstration in isolated monocytes from cystic fibrosis patients[J]. J Immunol, 2009, 182(10): 6494－6507.
[6]	马海鹰. 内毒素耐受小鼠Toll样受体2, 4及其下游分子Tollip蛋白表达变化的研究[D]. 南京：东南大学，2005.
[7]	Zhang N, Yu S, Liu X, et al. Low dose of lipopolysaccharide pretreatment preventing subsequent endotoxin－induced uveitis is associated with PI3K/AKT pathway[J]. J Immunol Res, 2017, PMID: 28804726.
[8]	Poltorak A, He X, Smirnova I, et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 Gene[J]. Science, 1998, 282(5396): 2085－2088.
[9]	Nagai Y, Akashi S, Nagafuku M, et al. Essential role of MD－2 in LPS responsiveness and TLR4 distribution[J]. Nat Immunol, 2002, 3: 667－672.
[10]	Yang H, Wang H, Ju Z, et al. MD－2 is required for disulfide HMGB1－dependent TLR4 signaling[J]. J Exp Med, 2015, 212(1): 5－14.
[11]	Kim HM, Kim YM. HMGB1: LPS delivery vehicle for caspase－11－mediated pyroptosis[J]. Immunity, 2018, 49(4): 582－584.
[12]	Manĉek－Keber M, Jerala R. Postulates for validating TLR4 agonists[J]. European J Immunol, 2015, 45(2): 356－370.
[13]	Chen W. Expression of toll－like receptor 4 in uvea－resident tissue macrophages during endotoxin－induced uveitis[J]. Mol Vis, 2009, 15(63): 619－628.
[14]	李上，卢弘，陈巍，等. TLR－4和CD14在急性前葡萄膜炎小鼠虹膜中的表达[J]. 眼科新进展，2010，30(1)：6.
[15]	Schumann RR. Old and new findings on lipopolysaccharide－binding protein: a soluble pattern－recognition molecule[J]. Biochem Soc Trans, 2011, 39(4): 989－993.
[16]	Kim SJ, Kim HM. Dynamic lipopolysaccharide transfer cascade to TLR4/MD2 complex via LBP and CD14[J]. Bmb Rep, 2017, PMID: 28115037.
[17]	Medzhitov R. Approaching the Asymptote: 20 Years Later[J]. Immunity, 2009, 30(6): 766－775.
[18]	Prohinar P, Re F, Widstrom R, et al. Specific high affinity interactions of monomeric endotoxin·protein complexes with Toll－like receptor 4 ectodomain[J]. J Biol Chem, 2007, 282(2): 1010－1017.
[19]	Gioannini TL, Teghanemt A, Zhang DS, et al. Isolation of an endotoxin－MD－2 complex that produces Toll－like receptor 4－dependent cell activation at picomolar concentrations[J]. Proc Natl Acad Sci U S A, 2004, 101(12): 4186－4191.
[20]	Gioannini TL, Teghanemt A, Zhang D, et al. Monomeric endotoxin: protein complexes are essential for TLR4－dependent cell activation[J]. J Endotoxin Res, 2005, 11(2): 117.
[54]	Van TVC, Van DPPS, Van－Zoelen MAD, et al. Induction of IRAK－M is associated with lipopolysaccharide tolerance in a human endotoxemia model[J]. J Immunol, 2007, 179(10): 7110－7120.
[55]	Yu S, Liu X, Zhang N, et al. Protection of Lipopolysaccharide (LPS) preconditioning against Endotoxin－Induced Uveitis (EIU) in rats is associated with overexpression of interleukin－1 receptor－associated kinase M(IRAK－M)[J]. Ocul Immunol Inflamm, 2018, PMID: 28609207.
[56]	Ling Y, Wang J, Yu S, et al. The protective effect of low dose of lipopolysaccharide pretreatment on endotoxin－induced uveitis in rats is associated with downregulation of CSF－1 and upregulation of LRR－1[J]. J Immunol Res, 2020, PMID: 32671118.

Please choose a citation manager

Content to export