Differential expression of Toll-like receptors and inflammatory cytokines in ovine interdigital dermatitis and footrot.
Differential expression of Toll-like receptors and inflammatory cytokines in ovine interdigital dermatitis and footrot.
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DOI：
10.1016/j.vetimm.2014.07.007
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发表时间：
2014-09-15
影响因子：
1.8
通讯作者：
Tötemeyer S
中科院分区：
文献类型：
--
作者：
Davenport R;Heawood C;Sessford K;Baker M;Baiker K;Blacklaws B;Kaler J;Green L;Tötemeyer S
蹄病是一种常见的炎性细菌性疾病，影响全世界绵羊的健康和福利。足腐病的发病机制是复杂和多因素的。主要的致病病原体是厌氧细菌结节叉鞭金杆菌，坏死梭杆菌也显示在疾病中发挥关键作用。由于涉及免疫介导的病理学，本研究的目的是调查宿主反应在趾间皮炎（ID）和蹄病中的作用。我们比较了Toll样受体（TLR）和促炎细胞因子的表达和临床正常的组织学外观相比，ID和足炎受影响的组织。重度ID和足癣的特征是趾间皮肤中促炎细胞因子TNFα和IL 1 β以及模式识别受体TLR 2和TLR 4的转录水平显著增加。这反映在组织病理学外观中，ID和足炎表现为进行性慢性活动性足皮炎，伴有混合淋巴细胞和嗜中性粒细胞浸润，从临床正常足的轻度形式逐渐增加到ID的中度形式，再到足炎的局灶性重度形式，伴有频繁的化脓区域。用F. necrophorum和/或D.结节虫提取物表明，真皮成纤维细胞（真皮的驻留细胞类型）也通过增加TNFα、IL 1 β和TLR 2的表达而促进对腐蹄菌的炎症反应。总的来说，ID和足炎导致局部炎症反应，因为TLR和IL 1 β的表达水平取决于足部的疾病状态而不是动物。
Footrot is a common inflammatory bacterial disease affecting the health and welfare of sheep worldwide. The pathogenesis of footrot is complex and multifactorial. The primary causal pathogen is the anaerobic bacterium Dichelobacter nodosus, with Fusobacterium necrophorum also shown to play a key role in disease. Since immune-mediated pathology is implicated, the aim of this research was to investigate the role of the host response in interdigital dermatitis (ID) and footrot. We compared the expression of Toll-like receptors (TLRs) and pro-inflammatory cytokines and the histological appearance of clinically normal in comparison to ID and footrot affected tissues. Severe ID and footrot were characterised by significantly increased transcript levels of pro-inflammatory cytokines TNFα and IL1β and the pattern recognition receptors TLR2 and TLR4 in the interdigital skin. This was reflected in the histopathological appearance, with ID and footrot presenting progressive chronic-active pododermatitis with a mixed lymphocytic and neutrophilic infiltration, gradually increasing from a mild form in clinically normal feet, to moderate in ID and to a focally severe form with frequent areas of purulence in footrot. Stimulation with F. necrophorum and/or D. nodosus extracts demonstrated that dermal fibroblasts, the resident cell type of the dermis, also contribute to the inflammatory response to footrot bacteria by increased expression of TNFα, IL1β and TLR2. Overall, ID and footrot lead to a local inflammatory response given that expression levels of TLRs and IL1β were dependent on the disease state of the foot not the animal.
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影响因子：
5.5
作者：
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影响因子：
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作者：
Nalubarnba, King S.;Gossner, Anton G.;Hopkins, John
通讯作者：
Hopkins, John