A protective role of Complement component 3 in Imiquimod induced Psoriasis-Like skin Inflammation
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- 英文论文题名：A protective role of Complement component 3 in Imiquimod induced Psoriasis-Like skin Inflammation
- 论文作者：Zheng Quanyou ; Li Guiqing ; Zhang Keqin ; Xu Guilian
- 英文论文作者：Zheng Quanyou ; Li Guiqing ; Zhang Keqin ; Xu Guilian ; Department of Immunology ; Third Military Medical University ; Department of Nephrology ; Southwest Hospital ; Third Military Medical University
- 年：2016
- 作者机构：Department of Immunology,Third Military Medical University;Department of Nephrology,Southwest Hospital,Third Military Medical University;
- 英文论文关键词：Psoriasis ; complement component 3 ; Imiquimod
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R758.63
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1329k
- 原文格式：D
- 会议级别：全国
摘要
Objective: Psoriasis is one of the most common chronic inflammatory skin diseases, with an estimated prevalence of about 2% of the population all over the world. Lacking understanding of its pathogenesis has in essence hindered efficient clinic treatment. Increasing reports indicate that the complement system performs a vital role in the development of psoriatic skin disorders. Here, we investigated the effect of complement component 3(C3) in the pathogenesis of psoriasis and explored the underlying mechanism utilizing the imiquimod(IMQ) induced psoriasis like skin inflammation model. Methods: The psoriatic skin inflammation was monitored and histological changes of skin were also assessed following 5 consecutive days of IMQ application. The expansion of inflammatory cells was analyzed by immune histological staining(IHC) and flow cytometry(FCM). The mRNA levels of inflammatory cytokines and chemotactic factors were also tested by qRT-PCR. At last, the expansion of Th1 and Th17 cells in the draining lymphocytes were further examined by FCM.Results: The psoriatic skin inflammation induced by IMQ in C3 deficient mice was clearly enhanced, compared with wild-type mice. At the microscopic level, C3 deficient mice showed a dramatic increase in keratinocytes proliferation, granulocytes and T cells infiltration. At the mRNA level, the absence of C3 strongly increased the expression of cytokines, chemotactic factors and keratin 10, which reflects hyper-proliferation responses of keratinocytes. In contrast to the increased expansion of Th1 cell, the response of Th17 cell was remarkably reduced in C3 deficient mice. Conclusion: These results provide a new insight into a novel protective role of C3 in IMQ induced psoriatic skin inflammation.
Objective: Psoriasis is one of the most common chronic inflammatory skin diseases, with an estimated prevalence of about 2% of the population all over the world. Lacking understanding of its pathogenesis has in essence hindered efficient clinic treatment. Increasing reports indicate that the complement system performs a vital role in the development of psoriatic skin disorders. Here, we investigated the effect of complement component 3(C3) in the pathogenesis of psoriasis and explored the underlying mechanism utilizing the imiquimod(IMQ) induced psoriasis like skin inflammation model. Methods: The psoriatic skin inflammation was monitored and histological changes of skin were also assessed following 5 consecutive days of IMQ application. The expansion of inflammatory cells was analyzed by immune histological staining(IHC) and flow cytometry(FCM). The mRNA levels of inflammatory cytokines and chemotactic factors were also tested by qRT-PCR. At last, the expansion of Th1 and Th17 cells in the draining lymphocytes were further examined by FCM.Results: The psoriatic skin inflammation induced by IMQ in C3 deficient mice was clearly enhanced, compared with wild-type mice. At the microscopic level, C3 deficient mice showed a dramatic increase in keratinocytes proliferation, granulocytes and T cells infiltration. At the mRNA level, the absence of C3 strongly increased the expression of cytokines, chemotactic factors and keratin 10, which reflects hyper-proliferation responses of keratinocytes. In contrast to the increased expansion of Th1 cell, the response of Th17 cell was remarkably reduced in C3 deficient mice. Conclusion: These results provide a new insight into a novel protective role of C3 in IMQ induced psoriatic skin inflammation.
Objective: Psoriasis is one of the most common chronic inflammatory skin diseases, with an estimated prevalence of about 2% of the population all over the world. Lacking understanding of its pathogenesis has in essence hindered efficient clinic treatment. Increasing reports indicate that the complement system performs a vital role in the development of psoriatic skin disorders. Here, we investigated the effect of complement component 3(C3) in the pathogenesis of psoriasis and explored the underlying mechanism utilizing the imiquimod(IMQ) induced psoriasis like skin inflammation model. Methods: The psoriatic skin inflammation was monitored and histological changes of skin were also assessed following 5 consecutive days of IMQ application. The expansion of inflammatory cells was analyzed by immune histological staining(IHC) and flow cytometry(FCM). The mRNA levels of inflammatory cytokines and chemotactic factors were also tested by qRT-PCR. At last, the expansion of Th1 and Th17 cells in the draining lymphocytes were further examined by FCM.Results: The psoriatic skin inflammation induced by IMQ in C3 deficient mice was clearly enhanced, compared with wild-type mice. At the microscopic level, C3 deficient mice showed a dramatic increase in keratinocytes proliferation, granulocytes and T cells infiltration. At the mRNA level, the absence of C3 strongly increased the expression of cytokines, chemotactic factors and keratin 10, which reflects hyper-proliferation responses of keratinocytes. In contrast to the increased expansion of Th1 cell, the response of Th17 cell was remarkably reduced in C3 deficient mice. Conclusion: These results provide a new insight into a novel protective role of C3 in IMQ induced psoriatic skin inflammation.
引文