|
|
|
| Tim-3信号通路调控巨噬细胞极化在鲍曼不动杆菌性肺炎免疫致病和免疫防治中的作用 |
| 王慧, 王萌, 张啸 |
| 南昌大学第二附属医院,江西 南昌 330000 |
|
|
|
|
摘要 目的 探讨T细胞免疫球蛋白及粘蛋白-3（T-cell Ig-mucin-3,Tim-3）信号通路调控巨噬细胞极化在鲍曼不动杆菌性肺炎免疫致病和免疫防治中的作用。方法 选取正常小鼠,定为正常组20只,将小鼠感染为鲍曼不动杆菌毒性临床菌株和疫苗菌株,检查生存率,细菌定量,组织病理等,用Real-time PCR检测细胞因子,用流式检测BALF炎症细胞浸润,分别建立小鼠鲍曼不动杆菌肺炎模型组20只和鲍曼不动杆菌疫苗接种模型组20只。通过ELISA法、Western blot技术检测Tim-3信号通路抑制巨噬细胞极化方向的影响。结果 与正常组相比,临床株组IL-1β、TNF-α、IL-6、TGF-β显著升高（P<0.05）,与临床株组相比疫苗组IL-1β、TNF-α、IL-6、TGF-β显著降低（P<0.05）,差异有统计学意义。正常组肺组织结构正常,无明显病变;临床株组肺组织肺泡结构受损严重,可见血管充血、炎性细胞浸润等现象;与临床株组相比,疫苗组肺组织结构损坏得到缓解。临床株组与正常组比较鲍曼不动杆菌性肺炎性老鼠肺组织巨噬细胞的MI标记基因TNF-a的表达有所减少,但CD32的表达有所增加。M2标记基因CD206和IL-10的表达增加（p）（P<0.05）;Tim-3通路抑制巨噬细胞后CD32、TNF-α基因的相对表达量升高,CD206表达升高,IL-10表达降低（P<0.05）。结论 Tim-3信号通路调控巨噬细胞极化方向,在鲍曼不动杆菌性肺炎致病中起到免疫防治作用。
|
|
| 关键词 ：
Tim-3信号通路,
巨噬细胞极化,
鲍曼不动杆菌性肺炎,
免疫致病,
防治
|
|
收稿日期: 2024-03-05
|
|
|
| 基金资助:江西省卫生健康委科技计划项目（202210652） |
|
通讯作者:
张啸
|
[1] Morris FC,Dexter C,Kostoulias X,et al.2019.The Mechanisms of Disease Caused byAcinetobacter baumannii.Frontiers in microbiology 10:1601-1601.
[2] Patamatamkul S,Klungboonkrong V,Praisarnti P,et al.2017.A case-control study of community-acquired Acinetobacter baumannii pneumonia and melioidosis pneumonia in northeast Thailand:an emergingfatal disease with unique clinical features.Diagn Microbiol lnfect Dis 87:79-86.
[3] Roca l,Espinal P,Vila-Farres X,et al.2012.The Acinetobacter baumanni Oxymoron:Commensal HospitalDweller Turned Pan-Drug-Resistant Menace.Front Microbiol 3:148.
[4] Shlaes DM,Bradford PA.2018.Antibiotics-From There to Where:How the antibiotic miracle is threatenedby resistance and a broken market and what we can do about it.Pathog lmmun 3:19-43.
[5] 顾浩. 2019.鲍曼不动杆菌灭活全菌疫苗快速免疫保护效应及机制研究陆军军医大学.
[6] Netea MG,Schlitzer A,Placek K,et al.2019.Innate and Adaptive lmmune Memory:anEvolutionary Continuum in the Host's Response to Pathogens.Cell Host Microbe 25:13-26.
[7] Mitroulis l,Ruppova K,Wang B,Chen LS,Grzybek M,Grinenko T,Eugster A,Troullinaki M,Palladini AKourtzelis l,Chatzigeorgiou A,Schlitzer A,Beyer M,Joosten LAB,lsermann B,Lesche M,Petzold A,SimonsK,Henry l,Dahl A,Schultze JL,Wielockx B,Zamboni N,Mirtschink P,Coskun U,Hajishengallis G,Netea MGChavakis T.2018.Modulation of Myelopoiesis Progenitors ls an lntegral Component of Trained lmmunity.Cell172:147-161 e12.
[8] 曾茜. 2020.肺泡巨噬细胞在鲍曼不动杆菌疫苗快速免疫保护中的作用及分子机制研究陆军军医大学.
[9] Kopf H,de la Rosa GM,Howard OM,et al.Rapamycin inhibits differentiation of Th17 cells and promotesgeneration of Fox P3+T regulatory cells.lnt.lmmunopharmacol,2007,7：1819-1824.
[10] Masuko-kongo K,Berenbaum F,Humbert L,et al.Thirion,Up-regulation of microsomal prostaglandin Esynthase 1 in osteoarthritic human cartilage.Arthritis.Rheum,2004,50：2829-2838.
[11] Wang F,He WT,Yuan J,et al.Activation of Tim-3-Galectin-9 pathway improves survival of fully allogeneicskin grafts.Transpl.Immunol,2008,19:12-19.
[12] Zhang Y,Ma CJ,Wang JM,et al.Tim-3 regulates pro-and antiinflammatory cytokine expression in human CD14+monocytes/J1.J Leukoc Biol.2012.912):189-196.15.Xie YYu J,Zhou NJ,Mao ZR.The effect and mechanism of Tim3 over-expression on TLRs signaling pathway inmacrophages[J].J Gastroenterol Hepatol.2014,293(SI):28-29.
[13] Xie Y,Mao ZR,Zhou NJ,et al.The influence of Tim-3 on TLR4 pathways in RAW 264.7 infected with H.pylori[J].J Gastroenterol Hepatol.2014,293(SI):237
[14] Xie Y.The influence of blocking Tim-3 signal pathway on immune pathopoiesis of H.pylori infection andTLRs signal pathwayiJ].[J] Gastroenterol Hepatol.2011,265(SI):268.
[15] Xie Y,Gong YF,Liu W,et al.The infiuence of blocking Tim-3 signalpathway on immune protection of H.pylori vaccine and TLRs signalpathwaylJ].[J] Gastroenterol Hepatol.2010,252:A167-A168.
[16] Jiang X,Yu J,Shi Q,et al.Tim-3 promotes intestinal homeostasis in DSS colitis by inhibiting M1 polarization of macrophages[J].Clin lmmunol.2015,160(2):328-335. |
| [1] |
马静, 于兰, 李婷, 王林, 张晓琳, 李一. 黑龙江省高校大学生艾滋病认知状况及防控政策调查研究[J]. 哈尔滨医药, 2024, 44(2): 34-36. |
| [2] |
曾静, 吴龑, 曾庆. 影响种植体周围炎的相关因素及防治对策探析[J]. 哈尔滨医药, 2021, 41(3): 99-100. |
|
|
|
|
2024, Vol. 44 
