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白细胞介素1β和白细胞介素17在根尖周病组织肥大细胞上的表达 被引量:3

Expression of IL-1β and IL-17 on mast cells in human periapical diseases
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摘要 目的:观察不同类型慢性根尖周病组织中肥大细胞(mast cells,MCs)的分布情况,并分析白细胞介素1β(interleukin-1β,IL-1β)和白细胞介素17(interleukin-17,IL-17)在MCs上的表达情况,探讨MCs IL-1β和IL-17在根尖周病发病机制中的作用。方法:本实验共收集102例样本,分为3组:(1)根尖肉芽肿组32例;(2)根尖囊肿组35例;(3)正常对照组35例。组织标本经4%中性甲醛缓冲液固定48 h以上;石蜡包埋,组织连续切片,HE染色,在光学显微镜下观察其组织学改变;采用免疫荧光双染色法,在荧光显微镜下观察各组标本组织表达IL-1β和IL-17的MCs数目。结果:两组慢性根尖周病的炎症反应程度明显高于正常对照组(P<0.01);根尖囊肿组与根尖肉芽肿组之间炎症反应程度无显著差异(P>0.05)。与正常对照组相比,两组慢性根尖周病组织中IL-1β和IL-17阳性MCs数目均显著增多(P<0.01);根尖囊肿组与根尖肉芽肿组IL-1β和IL-17阳性MCs密度无显著性差异(P>0.05)。经Pearson相关分析,3组标本组织中IL-1β和IL-17阳性MCs密度与组织炎症反应程度存在直线的正相关关系(P<0.01)。结论:慢性根尖周病组织中MCs数目明显增多,同时IL-1β和IL-17阳性的MCs密度显著增高。IL-1β和IL-17阳性MCs密度与根尖周病的炎症程度趋势相一致。这提示IL-1β和IL-17阳性MCs可能在慢性根尖周病的致病机制中发挥重要作用。 AIM: To identify and quantify the expression of IL-1β and IL-17 in mast cells( MCs) in different types of human pericapical diseases using double immunofluorescence staining. METHODS: The specimens( n = 102),including healthy control( n = 35),periapical cyst( n = 35) and periapical granuloma( n = 32),were involved in the present study. The tissue samples were fixed in 10% buffered formalin for at least 48 h and then embedded in paraffin.Serial 5-μm-thick sections were deposited onto SuperFrost /Plus microscope glasses. Routine staining of the sections using hematoxylin eosin( HE) was performed for morphological evaluation. The number of IL-1β and IL-17 positive MCs was identified by double immunofluorescence staining. RESULTS: Compared with the healthy controls,the inflammation score of periapical lesions was significantly increased in the periapical patients( P 〈0. 01). The density of IL-1β and IL-17 positive MCs in the periapical lesions were obviously higher than that in the healthy controls( P〈 0. 01). However,no significant difference between periapical cyst and periapical granuloma was observed. The Pearson correlation analysis showed that there was a positive correlation between the density of IL-1β and IL-17 double positive MCs and inflammation score in different groups of specimens( P 〈0. 01). CONCLUSION: There is significantly increased number of MCs,along with increased density of IL-1β and IL-17 positive MCs in human periapical lesions. The increased density of IL-1β and IL-17 positive MCs has the similar tendency as the severity of tissue inflammation in human periapical lesions,suggesting that IL-1β and IL-17 positive MCs may play an important role in the pathogenesis of human periapical diseases.
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2014年第9期1666-1671,共6页 Chinese Journal of Pathophysiology
基金 广东省医学科研基金资助项目(No.A2013454)
关键词 慢性根尖周病 肥大细胞 白细胞介素类 Chronic periapical disease Mast cells Interleukins
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参考文献19

  • 1Sato K, Suematsu A, Okamoto K, et al. Thl7 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction [ J ]. J Exp Med, 2006, 203 ( 12 ) :2673-2682.
  • 2Ohyama H, Kato-Kogoe N, Kuhara A, et al. The involve- merit of IL-23 and the Thl7 pathway in periodontitis[ J]. J Dent Res, 2009, 88(7) :633-638.
  • 3Xiong H, Wei L, Peng B. Immunohistochemical localiza- tion of IL-17 in induced rat periapical lesions [ J ]. J Endod, 2009, 35(2) :216-220.
  • 4Beunk L, Verwoerd A, van Overveld F J, et al. Role of mast ceils in mucosal diseases: current concepts and strat- egies for treatment [ J ]. Expert Rev Clin Immunol, 2013, 9 ( 1 ) :53-63.
  • 5Shelburne CP, Abraham SN. The mast cell in innate and adaptive immunity[ J ]. Adv Exp Med Biol, 2011, 716 : 162-185.
  • 6Huang S, Lu F, Zhang Z, et al. The role of psychologic stress-induced hypoxia-inducible factor-lalpha in rat ex- perimental periodontitis [ J ]. J Periodontol, 2011, 82 (6) :934-941.
  • 7Bertolini DR, Nedwin GE, Bringman TS, el ah Stimula- tion of bone resorption and inhibition of bone formation in vitro by human tumor necrosis factors[J]. Nature, 1986, 319(6053) :516-518.
  • 8Ktnig A, Mlihlbauer RC, Fleisch H. Tumor necrosis fac- tor ot and interleukin-I simulate bone reso:rption in vivo measured by urinary [ 3H ] tetracycline excre!:ion from pre- labeled mice[J]. J Bone Miner Res, 1988, 3(6) :621- 627.
  • 9Sabatini M, Boyce B, Aufdemorte T, et al. Infusions of recombinant human interleukins 1 alpha and 1 beta cause hypercalcemia in normal mice[ J]. Proc Natl Acad Sei U S A, 19:88, 85(14) :5235-5239.
  • 10Wei S, Kawashima N, Suzuki N, et al. Kinetics of Thl7- related eytokine expression in experimentally induced rat periapieal lesions[J]. Aust Endod J, 2013, 39(3) : 164- 170.

二级参考文献46

  • 1Shea-Donohue T, Stiltz J, Zhao A, et al. Mast cells[ J ]. Curr Gastroenterol Rep, 2010,12(5) :349-357.
  • 2Zhang J, Alcaide P, Liu L, et al. Regulation of endotheli- al cell adhesion molecule expression by mast cells, macro- phages, and neutrophils [ J ]. PLoS One, 2011,6 ( 1 ) : e14525.
  • 3Maekem Oberti JP, Breser ML, Nufiez N, et al. Chemo- kine response induced by Chlamydia trachomatis in pros- tate derived CD4^ + and CD45^ - cells [ J ]. Reproduction, 2011,142 (3) :427-437.
  • 4Huang S, Lu F, Chen Y, et al. Mast cell degranulation in human periodontitis [ J ]. J Periodontol, 2013,84 ( 2 ) : 248- 255.
  • 5Armitage GC. Development of a classification system for periodontal diseases and conditions [ J ]. Ann Periodontol, 1999, 4:1-6.
  • 6Huang S, Lu F, Zhang Z, et al. The role of psychological stress induced hypoxia-inducible factor-1α in rat experi- mental periodontitis[ J]. J Periodontol, 2011,82 (6) :934- 941.
  • 7Iwasaki A, Medzhitov R. Toll-like receptor control of the adaptive immune responses [ J ]. Nat Immunol, 2004,5 (10) :987-995.
  • 8Hedayat M, Netea MG, Rezaei N. Targeting of Toll-like receptors: a decade of progress in combating infectious diseases[J]. Lancet Infect Dis, 2011,11 (9) :702-712.
  • 9Wara-Aswapati N, Chayasadom A, Surarit R, et al. In- duction of Toll-like receptor expression by Porphyromonas gingivalis[ J]. J Periodontol, 2013,84(7) : 1010-1018.
  • 10Buduneli N,Ozcka O, Nalbantsoy A. Salivary and plast ma levels of Toll-like receptor 2 and Toll-like receptor 4 i1 chronic periodontitis [ J ]. J Periodontol, 2011,82 ( 6 ) 878-884.

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同被引文献46

  • 1赵秀敏,艾红军,常新.成骨细胞和破骨细胞的传导通路和相关因子[J].中国实用口腔科杂志,2009,2(3):176-179. 被引量:16
  • 2谢晓莉,唐瞻贵,王静,刘虹,吴颖芳.根尖周炎治疗前后根管渗出液中IL-1β变化及意义[J].临床口腔医学杂志,2004,20(6):338-339. 被引量:1
  • 3何朝阳.慢性根尖周炎治疗体会[J].重庆医学,2005,34(3):355-355. 被引量:4
  • 4刘彦平,赵淑兰,孙燕燕,何志红.根尖周炎厌氧菌培养结果分析[J].实用口腔医学杂志,1996,12(2):112-113. 被引量:19
  • 5Ripka S, Kanig A, Buchholz M, et al.WNT5A-target of CUTL1 and potent modulator of tumor cell migration and invasion in pancreatic cancer [J].Carcinogenesis, 2007, 28(6): 1178-1187.
  • 6Katoh M, Katoh M. STAT3-induced WNT5A signaling loop in embryonic stem cells, adult normal tissues, chronic persistent inflammation, rheumatoid arthritis and cancer [J].Int J Mol Med, 2007, 19(2): 273-278.
  • 7Malgor R, Bhatt PM, Connolly BA, et al. Wnt5a,TLR2 and TLR4 are elevated in advanced human atherosclerotic lesions [J].Inflamm Res, 2014, 63(4): 277-285.
  • 8Nanbara H, Wara-aswapati N, Nagasawa T, et al. Modulation of Wnt5a expression by periodontopathic bacteria [J]. PLOS One, 2012, 7(4): e34434.
  • 9Riedemann NC, Guo RF, Ward PA.Novel strategies for the treatment of sepsis [J]. Nat Med, 2003, 9(5): 517-524.
  • 10Kabashima H, Nagata K, Maeda K, et al. Involvement of substance P, mast cells, TNF-alpha and ICAM-1 in the infiltration of inflammatory cells in human periapical granulomas [J]. J Oral Pathol Med, 2002, 31(3): 175-180.

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