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呼吸道病毒感染会促使趋化因子表达并加剧哮喘反应。

Respiratory viral infections drive chemokine expression and exacerbate the asthmatic response.

作者信息

Schaller Matthew, Hogaboam Cory M, Lukacs Nicholas, Kunkel Steven L

机构信息

Department of Pathology, University of Michigan Medical School, 109 Zina Pitcher Place, Ann Arbor, MI 48109, USA.

出版信息

J Allergy Clin Immunol. 2006 Aug;118(2):295-302; quiz 303-4. doi: 10.1016/j.jaci.2006.05.025.

DOI:10.1016/j.jaci.2006.05.025
PMID:16890750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7172995/
Abstract

A number of investigations have linked respiratory viral infections and the intensity and subsequent exacerbation of asthma through host response mechanisms. For example, it is likely that the immune-inflammatory response to respiratory syncytial virus can cause a predisposition toward an intense inflammatory reaction associated with asthma, and adenovirus might cause exacerbation of the immune response associated with chronic obstructive pulmonary disease. In each of these situations, the host's immune response plays a critical mechanistic role through the production of certain cytokines and chemokines. Specific aspects of these augmented immune responses are determined by the biology of the virus, the genetic variability of the host, and the cytokine-chemokine phenotype of the involved tissue. For instance, the type 1/type 2 cytokine ratio in the airways during infection with rhinovirus determines how long the viral infection endures. By this same theory, it has been demonstrated that chemokine levels produced during respiratory syncytial virus infection determine host responses to later immune stimuli in the lung, with the potential to augment the asthmatic response. Further research in this area will clarify cytokines, chemokines, or cell targets, which will provide the basis for next-generation therapies.

摘要

多项研究通过宿主反应机制将呼吸道病毒感染与哮喘的严重程度及随后的病情加重联系起来。例如,对呼吸道合胞病毒的免疫炎症反应很可能会导致机体易于出现与哮喘相关的强烈炎症反应,而腺病毒可能会使与慢性阻塞性肺疾病相关的免疫反应加重。在上述每种情况中,宿主的免疫反应通过产生某些细胞因子和趋化因子发挥关键的机制性作用。这些增强的免疫反应的具体方面由病毒的生物学特性、宿主的基因变异性以及所涉及组织的细胞因子 - 趋化因子表型决定。例如,感染鼻病毒期间气道中的1型/2型细胞因子比例决定了病毒感染持续的时间。基于同样的理论,已证明呼吸道合胞病毒感染期间产生的趋化因子水平决定了宿主对肺部后续免疫刺激的反应,有可能增强哮喘反应。该领域的进一步研究将阐明细胞因子、趋化因子或细胞靶点,这将为下一代治疗提供基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/da85d65a3110/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/09419a600583/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/305664c7cdb2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/da85d65a3110/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/09419a600583/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/305664c7cdb2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/649e/7172995/da85d65a3110/gr3.jpg

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