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循环氧化酶-2/前列腺素E2通路协调感染性支气管炎病毒在的气管扩张中的复制

Motamed Elsayed Mahmoud^1,2, Ahmed Ali^1,3, Muhammad Farooq¹

¹Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada.

Microbiology spectrum

|October 29, 2024

概括

感染性支气管炎病毒 (IBV) 在气管中的致病性涉及COX-2/PGE2通路,不同的IBV菌株诱导不同的免疫反应. 准这种途径为控制家禽IBV感染提供了潜力.

科学领域:

禽类免疫学禽类免疫学
病毒学病毒学
分子病原体的产生.

背景情况:

传染性支气管炎病毒 (IBV) 在家禽行业造成重大经济损失.
了解气管中的局部免疫反应对于有效的疾病控制至关重要.
诱导性循环氧化酶-2 (COX-2) 和前列腺素E2 (PGE2) 在IBV病变发生中的作用需要进一步阐明.

研究的目的:

调查COX-2和PGE2在气管器官培养 (TOC) 中IBV局部病原发生的作用.
为了比较两种不同的IBV菌株 (呼吸 Conn A5968和病原性DMV/1639) 对气管组织的影响.
评估向COX-2/PGE2和JAK-STAT通路的治疗潜力.

主要方法:

的气管器官培养 (TOC) 被IBV菌株感染.
使用实时PCR和免疫组织化学量化IBV基因组负载和抗原表达的量化.
测量了COX-2,PGE2,炎症性细胞因子 (IFN-α,IFN-β,IL-1β,IL-6) 和iNOS的表达.
使用各种治疗方法,包括COX-2抗剂 (SC-236),PGE2和途径抑制剂.

主要成果:

根据病毒菌株,IBV感染导致COX-2表达和PGE2产生不同的模式.
康纳A5968诱导了持续的COX-2表达和PGE2产生,并减少了炎症性细胞因子.
DMV/1639引起了短暂的COX-2表达和PGE2产生,并增加了炎症反应.
针对COX-2/PGE2和JAK通路的治疗减少了病毒载量和病变,而外源性PGE2则加剧了感染.

结论:

COX-2/PGE2通路在气管中的IBV局部病原发生中发挥着重要作用.
不同的IBV菌株通过不同的机制调节宿主免疫反应,涉及COX-2和PGE2.
抑制COX-2/PGE2和JAK-STAT通路的抑制剂显示出作为治疗IBV感染的治疗剂的前景.

关键词:

亚努斯酶抑制剂的使用循环氧基因酶 2 的作用.感染性支气管炎病毒感染性支气管炎病毒干扰素-γ-γ 的作用.它们包括interleukins.的前列腺素E2E2的前列腺素.前列腺素受体对抗剂前列腺素受体对抗剂选择性循环氧化原酶-2 抑制剂气管器官培养器官培养器官的气管

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