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沙门氏菌会操纵宿主,通过诱导介质素1β诱导引起病原性

Mor Zigdon¹, Jasmin Sawaed¹, Lilach Zelik¹

¹Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.

|January 18, 2024

概括

介素1β (IL-1β) 生产在沙门氏菌感染期间是有害的,增加死亡率. 阻断IL-1β信号传递通过调节免疫应答和补充系统,防止沙门氏菌肠道殖民和败血症.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
胃肠病学胃肠病学

背景情况:

与沙门氏菌 (Salmonella Typhimurium) 等病原体发生的急性胃肠道感染会诱导白素1β (IL-1β) 的释放.
在对沙门氏菌的肠道防御中IL-1β的确切作用仍然不完全理解.

研究的目的:

研究IL-1β在宿主防御和沙门氏菌感染期间死亡率中的作用.
阐明IL-1β影响肠道炎症,开始性微生物群和病原体扩张的机制.

主要方法:

利用IL-1β淘汰 (IL-1β -/-) 小鼠来评估IL-1β缺乏对沙门氏菌感染结果的影响.
分析了中性细胞的招募,肠道组织损伤,短链脂肪酸 (SCFA) 生产的共生种群和上皮细胞代谢.
研究了IL-1β,补充系统组件 (亚纳菲拉毒素,CPN1) 和宿主死亡率之间的相互作用.
在人类败血症患者中,与补充受体表达相关的IL-1β表达.

主要成果:

在沙门氏菌感染期间,IL-1β的产生被发现是有害的,使疾病恶化.
IL-1β -/-小鼠表现出中性粒细胞透率降低,组织损伤较小,并保留了SCFA生成的共生细胞.
缺少IL-1β可以防止表皮细胞中有利于病原体生长的代谢转变,从而抑制沙门氏菌的扩散.
IL-1β -/-小鼠显示出对死亡的保护,这与抑制的补充性亚菲拉托克素诱导和保存的碳氧酶N (CPN1) 活性有关.
在人类败血症患者中,IL-1β表达与补充受体表达相关.

结论:

沙门氏菌利用IL-1β信号来超越共生微生物并建立肠道殖民.
由IL-1β介导的补充性厌毒素的诱导和抑制CPN1是一个关键的途径,有助于侵袭性沙门氏菌的死亡率.
针对IL-1β信号传递和补充系统的交叉点,为侵入性沙门氏菌病提供了潜在的治疗策略.

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