• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文学位 >Bovine hoof horn ulcerative disease: Collateral tissue damage, inflammation, and inflammasome body activity
【24h】

Bovine hoof horn ulcerative disease: Collateral tissue damage, inflammation, and inflammasome body activity

机译：牛蹄角溃疡性疾病：附带组织损伤，炎症和身体炎症部分

获取原文
获取原文并翻译 | 示例
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We hypothesized inflammatory responses in the sole corium of bovine claws disturbed epidermal-dermal interactions. The objectives of this investigation were to (1) determine the effect of sterile and septic sole ulcer lesions on transcriptional expression of growth factors, signaling elements, AP-1 transcription factors and cell-cycle transition elements in epidermal-dermal tissues of the bovine sole corium, (2) determine the effect of sterile and septic sole ulcer lesions on transcriptional expression of markers of keratinocyte differentiation in the sole corium, (3) compare and contrast gene expression of products that orchestrate proliferative and differentiation programs in dermalepidermal elements of the ulcerated lateral claw sole corium, the lesion free medial claw sole corium from lame limbs, and the lateral claw sole corium of the completely normal limbs, and (4) determine the effect of sterile and septic sole ulcer lesions on inflammasome platform transcription, inflammasome body activation and induction of an interleukin 1 response. Tissues were obtained from mature, lactating, Holstein cows from the abattoir. Sole tissues from ulcerated lateral claws, the lesionless medial claw off the ulcerated limbs, and lateral claws of lesion-free hind limbs were excised. Groups included lesions associated with grades 2/3 or grades 4/5 ulcers. Transcripts were quantified by real-time polymerase chain reaction (RT-PCR) and data normalized to endogenous ubiquitin expression. No bacteria were recovered from ulcer lesions (n=6) of lateral claws with an intact sole horn and declared sterile. Cell-cycle transition elements cyclin D, cdk2, cdk4 and cdk6, the stem cell transcription factor p63, the tumor suppressor p21 and cell-cycle inhibitor sigma 14-3-3 were down-regulated in the ulcerated lateral claw and lesion free medial claw of the ulcerated limb. Similarly, PDGF, VEGF, GMCSF, KGF, IGF1 and IGF2, HB-EGF, and TGF-beta and their receptors PDGFR, KGFR, IGF1R, IGF2R and EGFR were down-regulated while GMCSFR was elevated in ulcers and lesion free medial sole coriums. The signal elements c-myc, fos, c-jun, junB, and junD were down-regulated across the ulcerated corium as well as the lesionless medial claw sole corium. Loricrin and involucrin were down-regulated in the ulcer and matching lesion-free medial claw. Cytokeratin 10 expression was diminished in the lesion while serine palmatoyl CoA transferase was diminished only in the medial claw. Cytokeratin 6 and beta1 integrin were elevated across the lesion and the medial claw. Disturbances in proliferative and differentiation mRNAs were associated with increased expression of metalloproteinase 2, metalloproteinase 9, IL-1beta, and IL-1 receptor antagonist in the ulcer. The biologically active cleavage products of both caspase-1 and IL-1beta were elevated in the lesion as well as the medial claw. Ulcer lesions of the corium associated with breached sole horn were contaminated with manure and considered septic. Expression of cdk4, cdk6, p21, and p63 were diminished across the center, margin and the surrounding uninvolved tissue of the septic ulcer as well as the medial claw. Cyclin D decreased across all three regions of the ulcer lesion and cdk2 was elevated across all zones of the lesion. Cyclin B increased in the ulcer center and the lesionless medial claw corium. KGF increased in all zones of the wound as well as in the medial claw. IGF1 increased in the uninvolved tissues proximal to the ulcer. VEGF, IGF2, HBEGF and receptors VEGFR, IGF1R, IGF2R, KGFR and EGFR were diminished across all regions of the ulcer as well as in the medial claw. TGF-alpha decreased in all regions of the lesion and medial claw except in tissue proximal to the wound. PDGF decreased in the uninvolved tissues next to the ulcer and the medial claw corium. GMCSFR increased across all regions of the ulcer and the medial claw. C-myc, fos, c-jun, and jun D decreased across all regions of the ulcer as well as the medial claw. JunB decreased in the medial claw. Involucrin, cytokeratin 14 ,cytokeratin 10 and transglutaminase decreased across all three regions of the ulcer. Similarly, serine palmatoyl CoA transferase 1 and 2 were also down-regulated in the medial claw as well as across the wound. Ceramide glycosyl transferase and loricrin decreased in the tissues adjacent to the ulcer and the medial claw. Bulbous pemphigus protein 180 (BP 180) was down-regulated in the center and margin while alpha6, beta1, and beta4 were decreased across all regions of the ulcer and the medial claw. Disturbances in proliferative and differentiation gene expression patterns were associated with increased metalloproteinase 2, IL-1RI and IL-1RII across all regions of the ulcer. Metalloproteinase 9 and IL-1alpha increased in the ulcer center while IL-1beta, pycard and caspase-1 increased in the ulcer center and margin. Septic ulcers demonstrated increased amounts of the biologically active caspase-1 and IL-1beta. These data indicate ulcer lesions in coriums of claws with intact sole horn are sterile inflammatory responses associated with inflammasome body and IL-1 activation, metalloproteinase expression and depressed proliferative and differentiative processes orchestrating wound repair and sole horn production. Ulcer progression leads to breached claw horn and septic inflammatory responses. Septic ulcers showed characteristic similar to that of non-healing, chronic wounding. Moreover, the lesion-free corium from medial claws showed patterns of expression in the same direction and often same magnitude as in the ulcer. Sole ulceration appears to begin with sterile inflammatory responses that sufficiently disturb epidermal-dermal interactions orchestrating claw horn to generate open, septically inflamed, non-healing wounds. Similar patterns in the lesion-free medial claw indicate corium epidermal-dermal interactions are disturbed across both claws of the limb.
机译：我们假设在牛爪的唯一真皮中的炎症反应扰乱了表皮-真皮相互作用。这项研究的目的是（1）确定无菌和脓毒性足底溃疡病变对牛足表皮-真皮组织中生长因子，信号传导元件，AP-1转录因子和细胞周期过渡元件转录表达的影响皮质，（2）确定无菌和败血性单一溃疡病灶对唯一皮质中角质形成细胞分化标志物转录表达的影响，（3）比较和对比在溃疡的表皮成分中协调增生和分化程序的产物的基因表达外侧足底真皮、,足四肢无病变的内侧足底真皮和完全正常肢体的外侧足底真皮，以及（4）确定无菌和脓性足底溃疡病变对炎性平台转录，炎性体激活的影响和诱导白介素1反应。从屠宰场的成熟的，泌乳的荷斯坦奶牛获得组织。切除溃疡侧爪的组织，溃疡四肢的无损伤内侧爪，无损伤后肢的外侧爪。组包括与2/3级或4/5级溃疡相关的病变。通过实时聚合酶链反应（RT-PCR）对转录物进行定量，并将数据标准化为内源性泛素表达。从具有完整的唯一角的侧爪溃疡病变（n = 6）中未发现细菌，并宣布为无菌。在溃疡的外侧爪和无病变的内侧爪中，细胞周期过渡因子cyclin D，cdk2，cdk4和cdk6，干细胞转录因子p63，肿瘤抑制因子p21和细胞周期抑制剂sigma 14-3-3下调。四肢溃疡。同样，PDGF，VEGF，GMCSF，KGF，IGF1和IGF2，HB-EGF和TGF-beta及其受体PDGFR，KGFR，IGF1R，IGF2R和EGFR均被下调，而GMCSFR在溃疡和无病变的内侧唯一皮质中升高。在溃疡的皮质以及无损伤的内侧爪唯一的皮质中，信号元件c-myc，fos，c-jun，junB和junD下调。 Loricrin和Involucrin在溃疡和无病变的内侧爪中被下调。细胞角蛋白10表达在病变中减少，而丝氨酸棕榈酰辅酶A转移酶仅在内侧爪中减少。细胞角蛋白6和beta1整联蛋白在整个病变和内侧爪处升高。增殖和分化mRNA的紊乱与溃疡中金属蛋白酶2，金属蛋白酶9，IL-1β和IL-1受体拮抗剂的表达增加有关。 caspase-1和IL-1beta的生物活性裂解产物在病变以及内侧爪中均升高。与破裂的唯一角相关的皮质溃疡损伤被粪肥污染，被认为是败血症。 cdk4，cdk6，p21和p63的表达在化脓性溃疡以及中爪的中心，边缘和周围未累及的组织中减少。细胞周期蛋白D在溃疡病变的所有三个区域均降低，而cdk2在病变所有区域均升高。 Cyclin B在溃疡中心和无损伤的内侧爪状皮质中增加。在伤口的所有区域以及内侧爪中，KGF均增加。 IGF1在溃疡附近的未累及组织中增加。在溃疡的所有区域以及内侧爪中，VEGF，IGF2，HBEGF和受体VEGFR，IGF1R，IGF2R，KGFR和EGFR均降低。除了靠近伤口的组织外，TGF-α在病变和内侧爪的所有区域均降低。 PDGF在溃疡和内侧爪皮质旁未累及的组织中减少。 GMCSFR在溃疡和内侧爪的所有区域均增加。 C-myc，fos，c-jun和jun D在溃疡以及内侧爪的所有区域均下降。 JunB在内侧爪中减少。在溃疡的所有三个区域中，总蛋白，细胞角蛋白14，细胞角蛋白10和转谷氨酰胺酶均降低。同样，在内侧爪以及整个伤口中，丝氨酸棕榈酰辅酶A转移酶1和2也被下调。在溃疡和内侧爪附近的组织中神经酰胺糖基转移酶和洛瑞林减少。鳞茎天疱疮蛋白180（BP 180）在溃疡和内侧爪的所有区域中下缘均被下调，而alpha6，beta1和beta4则降低。增殖和分化基因表达模式的紊乱与溃疡所有区域中金属蛋白酶2，IL-1RI和IL-1RII的增加有关。金属蛋白酶9和IL-1alpha在溃疡中心增加，而IL-1beta，溃疡中心和边缘的pycard和caspase-1增加。败血症性溃疡证明了具有生物活性的caspase-1和IL-1beta的含量增加。这些数据表明具有完整的足底角的爪的皮质中的溃疡病灶是与炎性体和IL-1活化，金属蛋白酶表达以及抑制伤口修复和足底产生的增殖和分化过程相关的无菌炎症反应。溃疡进展导致羊角角破裂和败血性炎症反应。败血症性溃疡表现出与无法愈合的慢性伤口相似的特征。而且，来自内侧爪的无损伤的皮质表现出与溃疡相同的方向和程度的表达模式。足底溃疡始于无菌的炎症反应，足以干扰表皮与皮肤的相互作用或协调羊角，从而产生开放的，感染性的，不愈合的伤口。无病灶内侧爪中的相似模式表明跨肢体的两个爪的皮质表皮-真皮相互作用受到干扰。

著录项

  • 作者

    Reeder, Trista Lynn.;

  • 作者单位

    University of Delaware.;

  • 授予单位 University of Delaware.;
  • 学科 Animal sciences.
  • 学位 Ph.D.
  • 年度 2012
  • 页码 218 p.
  • 总页数 218
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号