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经血逆流学说是目前最广为接受的子宫内膜异位症发病机制学说,但是与子宫内膜异位症实际发病率却不相符合。菌群微生态是近年来的研究热点。阴道菌群失调易位会导致脂多糖随逆流的经血进入女性腹腔,诱发腹腔内慢性低度炎症和免疫抑制环境,促进子宫内膜异位症的发生发展。基于此,本文通过综述现有脂多糖与子宫内膜异位症相关研究,进一步完善经血逆流学说。
Abstract:The theory of retrograde menstruation is the most widely accepted theory of endometriosis(EMs)pathogenesis,but it is not consistent with actual incidence of EMs. Microflora microecology is a research hotspot in recent years. The evidence shows that the dysfunctional translocation of vaginal flora will lead to lipopolysaccharide(LPS)flowing into the abdominal cavity of women with retrograde menstruation,which induce chronic low-grade inflammation and immunosuppressive environment in the abdominal cavity and promote the occurrence and development of EMs. Based on this,this paper further improved the theory of retrograde menstruation by reviewing the existing researches on LPS and EMs.
[1] Mori T,Ito F,Koshiba A.Local estrogen formation and its regulation in endometriosis[J].Reprod Med Biol,2019,18:305-311.
[2] Llarena NC,Falcone T,Flyckt RL.Fertility preservation in women with endometriosis[J].Clin Med Insights Reprod Health,2019,3:1-8.
[3] McCluggage WG.Endometriosis-related pathology:a discussion of selected uncommon benign,premalignant and malignant lesions[J].Histopathology,2020,76:76-92.
[4] Koninckx PR,Ussia A,Adamyan L,et al.Pathogenesis of endometriosis:the genetic/epigenetic theory[J].Fertil Steril,2019,111:327-340.
[5] 中国医师协会妇产科医师分会子宫内膜异位症专业委员会,中华医学会妇产科学分会子宫内膜异位症协作组.子宫内膜异位症长期管理中国专家共识[J].中华妇产科杂志,2018,53:836-841.
[6] Sweeney RP,Lowary TL.New insights into lipopolysaccharide assembly and export[J].Curr Opin Chem Biol,2019,53:37-43.
[7] Young VB.The role of the microbiome in human health and disease:an introduction for clinicians[J].BMJ,2017,356:j831.
[8] Khan KN,Kitajima M,Inoue T,et al.Additive effects of inflammation and stress reaction on Toll-like receptor 4-mediated growth of endometriotic stromal cells[J].Hum Reprod,2013,28:2794-2803.
[9] Keyama K,Kato T,Kadota Y,et al.Lipopolysaccharide promotes early endometrial-peritoneal interactions in a mouse model of endometriosis[J].J Med Invest,2019,66:70-74.
[10] Leyva-Gómez G,Prado-Audelo MLD,Ortega-Peňa S,et al.Modifications in vaginal microbiota and their influence on drug release:challenges and opportunities[J].Pharmaceutics,2019,11:e217.
[11] Gupta S,Kakkar V,Bhushan I.Crosstalk between vaginal microbiome and female health:a review[J].Microb Pathog,2019,136:103696.
[12] Ma D,Chen Y,Chen T.Vaginal microbiota transplantation for the treatment of bacterial vaginosis:a conceptual analysis[J].FEMs Microbiol Lett,2019,366:1-8.
[13] Muhleisen AL,Herbst-Kralovetz MM.Menopause and the vaginal microbiome[J].Maturitas,2016,91:42-50.
[14] Peric A,Weiss J,Vulliemoz N,et al.Bacterial colonization of the female upper genital tract[J].Int J Mol Sci,2019,20:E3405.
[15] Lin WC,Chang CY,Hsu YA,et a1.Increased risk of endometriosis in patients with lower genital tract infection:a nationwide cohort study[J].Medicine(Baltimore),2016,95:e2773.
[16] Fauconnier A,Chapron C.Endometriosis and pelvic pain:epidemiological evidence of the relationship and implications[J].Hum Reprod Update,2005,11:595-606.
[17] Kruitwagen RFPM,Poels LG,WillEMsen WNP,et al.Endometrial epithelial cells in peritoneal fluid during the early follicular phase[J].Fertil Steril,1991,55:297-303.
[18] Cao X,Yang DZ,Song MQ,et al.The presence of endometrial cells in the peritoneal cavity enhances monocyte recruitment and induces inflammatory cytokines in mice:implications for endometriosis[J].Fertil Steril,2004,82:999-1007.
[19] Khan KN,Kitajima M,Hiraki K,et al.Escherichia coli contamination of menstrual blood and effect of bacterial endotoxin on endometriosis[J].Fertil Steril,2010,94:2860-3.e1-3.
[20] Yuan M,Li D,Zhang Z,et al.Endometriosis induces gut microbiota alterations in mice[J].Hum Reprod,2018,33:607-616.
[21] Chadchan SB,Cheng M,Parnell LA,et al.Antibiotic therapy with metronidazole reduces endometriosis disease progression in mice:a potential role for gut microbiota[J].Hum Reprod,2019,34:1106-1116.
[22] Takiishi T,Fenero CIM,Camara NOS.Intestinal barrier and gut microbiota:Shaping our immune responses throughout life[J].Tissue Barriers,2017,5:e1373208.
[23] 王嘉榕,李燕,孙红宾.脂多糖-针对革兰阴性菌的药物靶标[J].生物医学工程学杂志,2015,32:910-913.
[24] 莫婷,刘马峰,程安春.革兰氏阴性菌脂多糖运输系统的构成及作用机制[J].微生物学报,2018,58:1521-1530.
[25] Raetz CR,Whitfield C.Lipopolysaccharide endotoxins[J].Annu Rev Biochem,2002,71:635-700.
[26] Sakamoto Y,Harada T,Horie S,et al.Tumor necrosis factor-α-induced interleukin-8(IL-8)expression in endometriotic stromal cells,probably through nuclear factor-κB activation:gonadotropin-releasing hormone agonist treatment reduced IL-8 expression[J].J Clin Endocrinol Metab,2003,88:730-735.
[27] Iba Y,Harada T,Horie S,et al.Lipopolysaccharide promoted proliferation of endometriotic stromal cells via induction of tumor necrosis factor a and interleukin-8 expression[J].Fertil Steril,2004,82:1036-1042.
[28] Kobayashi A,Maegawa M,Yamamoto S,et al.The role of blood in early endometrial-peritoneal interactions in a syngeneic mouse model of endometriosis[J].Reprod Med Biol,2011,10:15-20.
[29] Azuma Y,Taniguchi F,Nakamura K,et al.Lipopolysaccharide promotes the development of murine endometriosis-like lesions via nuclear factor-kappa B pathway[J].Am J Reprod Immunol,2017,77:1-9.
[30] Asante A,Taylor RN.Endometriosis:the role of neuroangiogenesis[J].Annu Rev Physiol,2011,73:163-182.
[31] Capobianco A,Monno A,Cottone L,et al.Proangiogenic Tie2(+)macrophages infiltrate human and murine endometriotic lesions and dictate their growth in a mouse model of the disease[J].Am J Pathol,2011,179:2651-2659.
[32] Uz YH,Murk W,Bozkurt I,et al.Increased c-Jun N-terminal kinase activation in human endometriotic endothelial cells[J].Histochem Cell Biol,2011,135:83-91.
[33] Rakhila H,Girard K,Leboeuf M,et al.Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo:a plausible link to endometriosis development[J/OL].PLoS One,2014,9:e110434.
[34] Jeung IC,Chung YJ,Chae B,et al.Effect of helixor A on natural killer cell activity in endometriosis[J].Int J Med Sci,2015,12:42-47.
[35] Yang HL,Zhou WJ,Chang KK,et al.The crosstalk between endometrial stromal cells and macrophages impairs cytotoxicity of NK cells in endometriosis by secreting IL-10 and TGF-β[J].Reproduction,2017,154:815-825.
基本信息:
中图分类号:R711.71
引用信息:
[1]倪喆鑫,孙帅,程雯,等.腹腔内脂多糖污染在子宫内膜异位症发生发展过程中的作用[J].生殖医学杂志,2020,29(07):968-971.
基金信息:
国家自然科学基金资助项目(81774352,81703874,81503604,81573755);; 上海市中医药三年行动计划[ZY(2018-2020)-FWTX-1107]
2019-12-26
2019
2020-05-20
2020
2020-02-06
1
2020-07-15
2020-07-15