Correlation of ERAP Gene Polymorphism with Antibody Response Induced by Sequential Immunization of Polio Vaccine
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摘要:
目的 分析内质网氨肽酶(endoplasmic reticulum aminopeptidases,ERAP)基因多态性与脊髓灰质炎疫苗序贯免疫诱导的中和抗体应答的相关性。 方法 选取243名来自广西壮族自治区并完成2剂灭活脊髓灰质炎疫苗和1剂二价口服脊髓灰质炎减毒疫苗接种的壮族受试者,检测免前和基础免疫28 d血清中I、II、III型脊髓灰质炎中和抗体水平,采用TaqMan探针基因分型法对单核苷酸多态性(single nucleotide polymorphism,SNP)进行分型。共选择8个SNP位点,6个ERAP1基因(rs27037、rs27044、rs30187、rs26618、rs26653、rs3734016)和2个ERAP2基因(rs2549782、rs2248374),计算各SNPs的等位基因和基因型频率,分析各SNPs与各型抗体应答的相关性。 结果 在I型脊髓灰质炎抗体应答中,携带rs2549782-G和rs2248374-A等位基因个体抗体几何平均滴度(geometric mean titer,GMT)低于携带rs2549782-T和rs2248374-G等位基因个体[均为(11.590±1.979) vs (11.950±1.895),P = 0.031];rs2549782基因型GT和rs2248374基因型AG诱导的中和抗体低于rs2549782基因型TT和rs2248374基因型GG[均为(11.741±0.141) vs (12.378±0.157),P = 0.045]。 结论 ERAP2基因多态性可能影响脊髓灰质炎疫苗诱导的抗体水平。 Abstract:Objective To analyze the relationship between endoplasmic reticulum aminopeptidases (ERAP) gene polymorphisms and serum polio antibodies induced by sequential polio vaccine immunization. Methods A total of 243 Zhuang individuals were selected from the Guangxi Zhuang Autonomous Region who received two doses of inactivated polio vaccine and one dose of bivalent oral polio vaccine. Polio-neutralizing antibodies types I, II and III were tested from pre-immunization and 28 days after immunizations, and six ERAP1 and two ERAP2 SNPs were genotyped using TaqMan probe genotyping. The allele frequency and genotype frequency were calculated for each SNP, and the association between the SNPs and the polio antibody response was analyzed. Results It was found that individuals carrying the rs2549782-G andrs2248374-A allele of the ERAP1 gene had lower levels of type I polio-neutralizing antibodies compared to those carrying the T and G alleles, respectively (both of 11.590±1.979 vs 11.950±1.895, Padj = 0.031). In addition, it was observed that GT and AG genotypes of rs2549782 of rs2248374 exhibited lower GMT type I polio-neutralizing antibodies than those of TT and GG genotypes (both of 11.741±0.141 vs 12.378±0.157, Padj = 0.045). Conclusion Polio vaccine-induced antibody responses may be associated with ERAP2 gene polymorphism. -
在牙列拥挤的人类学调查中,中国人和日本人严重拥挤患病率较高[1]。牙列拥挤易发生在前牙区[2],且随年龄增加,拥挤加剧[3-4]。上颌唇向低位尖牙在前牙拥挤病例中高发,这与牙弓长度、宽度发育不足密切相关[5- 6]。Akram[7]在上颌唇向低位尖牙的CBCT研究中发现,上颌唇向低位尖牙因不能行使正常咬合功能,牙根较短,骨体积、颊侧骨密度比正常尖牙组减少。这不仅影响患者美观,也造成牙周组织的损伤,需进行正畸治疗。但唇向低位尖牙因其牙周退行性变,正畸治疗过程中受力更易发生牙龈退缩、牙槽骨吸收[8-9]。
牙齿受到各种内在、外在、动态、静态的机械力,这些力共同驱动和维持生理性牙槽骨生长发育和平衡。有动物研究表明,恢复咬合功能低下牙的咬合刺激可诱导骨附着、增加牙槽骨表面骨量。课题组提出设想在正畸之前给予患者力学干预,恢复其牙周组织活性再对其进行矫治,以减少牙槽骨丧失风险。如何给予适当的力干预?传统固定矫治技术中,弓丝形状、力学行为、牙齿运动情况间的关系并不十分明确。临床医师无法准确预测应施加矫治力值的大小。近年来,无托槽压膜式矫治器以其可精准施力,精确设计的优点,越来越被医生和患者接纳。为解决这一难题,课题组使用数字化技术设计矫治器施力干预上颌唇向低位尖牙后再行常规矫治,探索此干预措施能否降低牙槽骨吸收量,提高正畸安全性。
1. 资料与方法
1.1 研究对象及分组
1.1.1 研究对象
筛选自2021年10月至2023年8月到云南大学附属医院口腔正畸科就诊有上颌唇向低位尖牙的成年患者,且均在云南大学附属医院口腔临床中心拍摄CBCT,所有患者签署知情同意书,该研究通过医院伦理委员会审查(批准号:2021063)。纳入标准:(1)年龄≥18岁,恒牙列,牙根发育完成,根尖无暗影,牙冠形态完整规则;(2)牙周健康或牙周病控制良好;(3)上颌尖牙唇向低位(距离咬合平面2 mm以上)患者。排除标准:(1)无正畸、正颌治疗史、前牙牙体或修复治疗史;(2)无唇腭裂或全身系统性、怀孕、遗传性疾病史;(3)上颌尖牙无明显扭转,无外伤、囊肿或手术史。
1.1.2 研究对象分组
课题组选择用数字化设计干预矫治器,给予无咬合力接触的尖牙沿长轴方向压低0.1 mm,每日佩戴4 h,连续佩戴3个月后开始常规的固定或隐形矫治。与患者沟通交流,将愿意进行干预的患者纳入干预组,否则进入对照组。
1.2 研究方法
1.2.1 釉牙骨质界到牙槽嵴顶的距离(CEJ-AC)
纳入的患者,在治疗前及低位尖牙纳入牙弓后均进行CBCT检测(NNTviewer,New Tom,Italy),扫描视野15 cm×15 cm,电压110 KVp,电流3.83 Ma,曝光时间3.6 s,扫描层厚0.3 mm。
选取尖牙最大矢状截面为牙槽嵴顶与CEJ距离的测量平面(图1)。步骤如下:如图A在轴面上,使横轴与竖轴垂直且交点位于牙体中心;在B、C调节冠状面、矢状面上牙体长轴与竖轴的重叠,此时为牙根横截面积最大面,以矢状面 C为测量界面。
测量并记录纳入病例治疗前后唇向低位尖牙唇侧牙槽嵴顶与釉牙骨质界距离h1(图2)。同一测量者在1个月后重复测量,取2次测量结果的平均值。
1.2.2 牙龈生物型的临床检测
采用Kan[10]提出的牙周探针检测牙龈生物型的方法,即将William牙周探针插入龈沟内,观察牙周探针若能透过牙龈被看到则为薄龈型,否则为厚龈型。
1.3 统计学处理
对纳入的患者进行治疗前后CBCT测量,并对临床检测指标进行统计分析。采用 SPSS22.0软件对数据进行处理。计量资料以均数±标准差(
$ \bar{x} \pm s $ )表示,前后差异比较采用配对t检验,两组差异比较采用成组t检验;计数资料用n(%)表示。以P < 0.05为差异有统计学意义。2. 结果
2.1 一般情况
收集病例43例(牙数54颗),其中男性15例(牙数21颗),女性28例(牙数33颗),患者年龄18~40岁。分为常规矫治组和干预矫治组,常规矫治组26例(牙数32颗),其中男性8例(牙数11颗),女性18例(牙数21颗),患者年龄18~33岁;干预矫治组17例(牙数22颗),其中男性7例(牙数10颗),女性10例(牙数12颗),患者年龄18~40岁。
2.2 干预措施对釉牙骨质界到牙槽嵴顶的距离(CEJ-AC)的影响
矫治前2组无统计学差异,矫治后干预组CEJ-AC降低(P < 0.05),常规矫治组CEJ-AC不变,且干预矫治组干预前后CEJ-AC差值大于常规矫治组(P < 0.01),提示干预措施有效,见表1。
表 1 常规矫治矫治组和干预矫治组矫治前后CEJ-AC情况[($ \bar{x} \pm s $ ),mm]Table 1. CEJ-AC before and after treatment in the non-intervention group and the intervention group[($ \bar{x} \pm s $ ),mm]组别 n(颗) 治疗前 治疗后 治疗前后差值 t P 常规矫治组 32 3.30 ± 1.91 3.43 ± 1.63 −0.13 ± 0.11 −1.25 0.220 干预矫治组 22 3.63 ± 1.58 3.15 ± 1.32 0.48 ± 0.12 4.01 0.001* t −0.66 0.68 3.79 P 0.515 0.499 < 0.001* *P < 0.05。 2.3 牙龈生物型对CEJ-AC的影响
矫治前后,薄龈型低位尖牙患者的CEJ-AC变化,差异无统计学意义(P > 0.05),干预组厚龈型低位尖牙患者的CEJ-AC降低(P < 0.05),且变化值同常规矫治组相比,差异有统计学意义(P < 0.05),见表2。
表 2 干预措施对不同牙龈型矫治前后CEJ-AC的影响[($ \bar{x} \pm s $ ),mm]Table 2. Effect of interventions on CEJ-AC before and after treatment with different gingival type [($ \bar{x} \pm s $ ),mm]组别 n(颗) 治疗前 治疗后 治疗前后差值 t P 薄龈型 常规矫治组 19 3.32 ± 2.05 3.57 ± 1.71 −0.25 ± 0.16 −1.59 0.129 干预矫治组 12 3.39 ± 1.47 3.22 ± 1.31 0.18 ± 0.11 1.64 0.129 t −0.10 0.61 1.98 P 0.918 0.547 0.058 厚龈型 常规矫治组 13 3.28 ± 1.76 3.24 ± 1.55 0.04 ± 0.11 0.34 0.743 干预矫治组 10 3.91 ± 1.73 3.07 ± 1.39 0.84 ± 0.17 4.92 0.001* t −0.86 0.27 4.04 P 0.400 0.790 0.001* *P < 0.05。 2.4 矫治方式对CEJ-AC的影响
固定矫治的低位尖牙患者,干预组矫治后CEJ-AC值降低(P < 0.05),常规矫治组的CEJ-AC值变化差异无统计学意义(P > 0.05),干预组治疗前后的CEJ-AC差值大于常规矫治组(P < 0.05);隐形矫治的低位尖牙患者,干预组矫治后的CEJ-AC降低值大于常规矫治组(P < 0.05),见表3。
表 3 干预措施对不同矫治方式矫治前后CEJ-AC的影响[($\bar{x} \pm s $ ),mm]Table 3. Effect of interventions on CEJ-AC before and after treatment with different treatment methods [($\bar{x} \pm s $ ),mm]组别 n(颗) 治疗前 治疗后 治疗前后差值 t P 固定矫治 常规矫治组 26 3.38±1.88 3.47±1.61 0.10±0.11 0.81 0.428 干预矫治组 14 3.12±1.35 2.73±1.17 −0.39±0.10 −3.65 0.003* t 0.45 1.52 2.69 P 0.657 0.137 0.010* 隐形矫治 常规矫治组 6 2.98±2.17 3.27±1.84 0.28±0.22 1.27 0.259 干预矫治组 8 4.51±1.62 3.89±1.28 −0.63±0.27 −2.29 0.055 t −1.51 −0.75 2.45 P 0.156 0.470 0.030* *P < 0.05。 3. 讨论
牙列拥挤病例中非常常见的唇向低位尖牙属于咬合功能低下牙,失去正常咬合力的维持,其牙体牙周会出现如牙周膜和牙槽骨的退行性改变[11]。牙槽嵴顶的位置,即釉牙骨质界到牙槽嵴顶的距离(CEJ-AC)是正畸、正颌医师为规避牙周风险如牙龈退缩、牙槽骨吸收等十分关注的解剖因素[12]。研究认为CEJ-AC距离为2 mm以内[13]。有许多研究表明CBCT可准确提供牙周缺损的三维形态,优于传统的口腔X线片[14]。课题组选取的患者年龄在18~40岁,治疗前牙周情况均符合矫治标准,采用CBCT测量CEJ-AC,43例患者治疗前CEJ-AC的平均值为3.44 mm(95%CI:2.95~3.92),提示唇向低位尖牙牙槽嵴顶位置偏低,具有牙槽骨量不足的缺陷,在正畸过程中易出现牙槽骨吸收。这与课题组在前期的研究中发现,低位尖牙的患者正畸治疗后更容易出现牙龈退缩[9]结果相一致。
动物实验报道,咬合功能低下牙齿移动过程中PDL和血管细胞发生凋亡[15],牙周组织易发生退行性变。基础研究发现通过恢复咬合功能干预,牙周膜结构、松质骨和皮质骨骨密度有所恢复[8],还能通过增加 IGF-1和其受体诱导牙周膜细胞增殖[16]。数字化设计无托槽隐形矫治器有可精确施力的特点,课题组对上颌低位尖牙设计了干预措施:给予所选牙沿长轴方向压低0.1 mm的移动量的力,每日佩戴4 h,即给予牙齿间断力,连续佩戴3个月后开始常规矫治。这样牙周膜受轻力刺激,但基本不产生牙齿的移动。对照组则直接进行常规矫治。本研究选取上颌唇向低位尖牙进行研究,结果显示:干预措施组与常规矫治组治疗前CEJ-AC无组间差异;但矫治后,干预组CEJ-AC降低(P < 0.05),而常规矫治组CEJ-AC与矫治前无差别,提示干预措施有效,干预措施减少了上颌唇向低位牙矫治造成的牙槽骨量的丧失。
牙龈厚度是牙龈退缩发生的相关因素。Marziyeh 等[17]评估出牙龈生物型与牙槽骨厚度成正相关,牙龈越薄牙槽骨也越薄。而薄龈型患者正畸后牙龈退缩发生率更高[9,18]。课题组也探索了干预措施与牙龈生物型对治疗后牙槽骨丧失的作用,提示:干预措施对上颌厚牙龈型唇向低位牙牙槽骨吸收干预有效,对薄龈型未见明显效果。上颌薄龈型唇向低位尖牙患者对应更少的牙槽骨和牙龈量,在正畸力作用后,更容易发生缺失,尚需寻求其他干预措施提高正畸治疗的安全性。
固定矫治使用的托槽和弓丝等影响口腔清洁,引起菌斑积聚,易形成牙周组织炎症[19]。隐形矫治因其刷牙和进食可摘戴,对口腔清洁影响小,但其包裹性强,摘戴时产生力量大,对牙周的影响有争议[20]。在本研究中,干预措施运用于两种不同矫治方式的治疗中,发现固定矫治上颌低位尖牙患者,干预措施矫治后CEJ-AC值降低(P < 0.05),治疗前后的CEJ-AC差值大于常规矫治组(P < 0.05),提示干预措施有效;隐形矫治的低位尖牙患者,干预组矫治前后的CEJ-AC降低值大于常规矫治组(P < 0.05),也提示干预措施有效。
课题组通过对上颌唇向低位尖牙进行数字化设计无托槽矫治器进行治疗前干预,发现干预措施对厚龈型患者矫治后的CEJ-AC有改善作用,但对薄龈型无明显作用;在固定矫治或隐形矫治前进行干预,均有效果。
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表 1 SNPs的位点信息
Table 1. SNPs information
基因 SNP位点 位置 突变类型 ERAP1 rs27037(G/T) chr5:96758990 intron rs27044(C/G) chr5:96783148 Gln730Glu(Q>E) rs30187(C/T) chr5:96788627 Lys528Arg(K>R) rs26618(T/C) chr5:96795133 Ile276Met(I>M) rs26653(C/G) chr5:96803547 Arg127Pro(R>P) rs3734016(C/T) chr5:96803761 Glu56Lys(E>K) ERAP2 rs2549782(T/G) chr5:96895296 Lys392Asn(K>N) rs2248374(G/A) chr5:96900192 splice region variant 表 2 研究对象基本特征(
$\bar x \pm s $ )Table 2. Basic characteristics of the subjects (
$\bar x \pm s $ )型别 性别(n) GMT t P I型 男(128) 11.628 ± 2.043 1.350 0.178 女(115) 11.964 ± 1.814 II型 男(128) 6.110 ± 1.806 0.945 0.345 女(115) 6.335 ± 1.910 III型 男(128) 11.409 ± 1.699 1.292 0.198 女(115) 11.675 ± 1.492 表 3 ERAP基因的SNPs位点等位基因与脊灰中和抗体(GMT)水平的相关性(
$\bar x \pm s $ )Table 3. Correlation between ERAP SNPs alleles and GMT of neutralizing antibody against poliovirus (
$\bar x \pm s $ )基因 SNP位点 脊灰抗体型 等位基因 n GMT P ERAP1 rs27037 I G 295 11.860 ± 1.873 0.351 T 191 11.670 ± 2.038 II G 295 6.205 ± 1.765 0.961 T 191 6.233 ± 1.986 III G 295 11.600 ± 1.463 0.838 T 191 11.430 ± 1.801 rs27044 I C 252 11.870 ± 1.913 0.282 G 234 11.700 ± 1.968 II C 252 6.272 ± 1.733 0.416 G 234 6.156 ± 1.937 III C 252 11.620 ± 1.450 0.760 G 234 11.450 ± 1.755 rs30187 I C 249 11.860 ± 1.915 0.338 T 237 11.710 ±1.966 II C 249 6.297 ± 1.784 0.245 T 237 6.131 ± 1.923 III C 249 11.610 ± 1.467 0.815 T 237 11.460 ± 1.738 rs26618 I C 157 11.740 ± 1.902 0.579 T 329 11.810 ± 1.960 II C 157 6.277 ± 1.804 0.497 T 329 6.187 ± 1.878 III C 157 11.650 ± 1.410 0.657 T 329 11.480 ± 1.690 rs26653 I C 247 11.760 ± 1.947 0.657 G 239 11.820 ± 1.936 II C 247 6.114 ± 1.899 0.155 G 239 6.322 ± 1.802 III C 247 11.470 ± 1.725 0.910 G 239 11.800 ± 1.472 rs3734016 I C 428 11.730 ± 1.954 0.077 T 58 12.190 ± 1.792 II C 428 6.170 ± 1.858 0.129 T 58 6.558 ± 1.790 III C 428 11.510 ± 1.634 0.582 T 58 11.720 ± 1.374 ERAP2 rs2549782 I G 221 11.590 ± 1.979 0.031* T 265 11.950 ± 1.895 II G 221 6.187 ± 1.836 0.992 T 265 6.241 ± 1.870 III G 221 11.560 ± 1.578 0.943 T 265 11.510 ± 1.630 rs2248374 I A 221 11.590 ± 1.979 0.031* G 265 11.950 ± 1.895 II A 221 6.187 ± 1.836 0.992 G 265 6.241 ± 1.870 III A 221 11.560 ± 1.578 0.943 G 265 11.510 ± 1.630 *P < 0.05。 表 4 ERAP基因SNPs的基因型与脊灰I型中和抗体GMT水平的相关性(
$\bar x \pm s $ )Table 4. Correlation between ERAP SNPs genotypes and GMT of neutralizing antibody against polio type1 (
$\bar x \pm s $ )ERAP SNP位点 抗体型别 基因型 n GMT P ERAP1 rs27037 I型 GG 86 12.099 ± 1.792 0.109 GT 123 11.535 ± 1.948 TT 34 11.910 ± 2.202 rs27044 I型 CC 58 12.010 ± 2.001 0.563 CG 136 11.750 ± 1.841 GG 49 11.630 ± 2.150 rs30187 I型 CC 56 11.990 ± 2.033 0.626 CT 137 11.750 ± 1.822 TT 50 11.650 ± 2.167 rs26618 I型 CC 20 11.930 ± 1.591 0.672 CT 117 11.670 ± 2.005 TT 106 11.890 ± 1.939 rs26653 I型 CC 57 11.780 ± 2.083 0.830 CG 133 11.730 ± 1.839 GG 53 11.930 ± 2.064 rs3734016 I型 CC 189 11.690 ± 1.968 0.235 CT 50 12.080 ± 1.854 TT 4 12.900 ± 1.286 ERAP2 rs2549782 I型 GG 48 11.600 ± 2.046 0.043* GT 125 11.590 ± 1.942 TT 70 12.280 ± 1.802 rs2248374 I型 AA 48 11.600 ± 2.046 0.043* AG 125 11.590 ± 1.942 GG 70 12.280 ± 1.802 *P < 0.05。 -
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