百日咳杆菌对流感的百日咳毒素依赖性和非依赖性保护。

IF 2.6 4区医学 Q3 IMMUNOLOGY Microbes and Infection Pub Date : 2024-08-10 DOI:10.1016/j.micinf.2024.105404

Thomas Belcher, Loïc Coutte, Anne-Sophie Debrie, Valentin Sencio, François Trottein, Camille Locht, Stephane Cauchi

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引用次数: 0

摘要

细菌和病毒的合并感染很常见，但它们之间的相互影响却不甚了解。在这里，我们研究了百日咳杆菌感染和百日咳毒素（PT）对甲型流感病毒（IAV）感染和疾病的影响。在 C57BL/6J 小鼠中，事先经鼻给予毒性百日咳杆菌 BPSM 和 PT 缺失的 BPRA 可提供有效且持续的保护，防止 IAV 引起的死亡。然而，与单独使用 BPRA 相比，同时使用 BPSM 或 BPRA 和纯化 PT（BPRA+PT）对体重减轻有更强的保护作用，可减少病毒载量并诱导肺部 IL-17A。在IL-17-/-小鼠中，BPSM-和BPRA+PT介导的抗病毒复制保护作用被取消，而BPSM、BPRA和BPRA+PT对IAV诱导的死亡率和体重减轻提供了相似水平的保护。总之，百日咳杆菌感染可通过两种机制预防流感：一种机制依赖于PT和IL-17减少病毒复制，另一种机制则独立于PT和IL-17，在不减少病毒载量的情况下对流感疾病产生保护作用。

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Pertussis toxin-dependent and -independent protection by Bordetella pertussis against influenza.

Bacterial-viral co-infections are frequent, but their reciprocal effects are not well understood. Here, we examined the effect Bordetella pertussis infection and the role of pertussis toxin (PT) on influenza A virus (IAV) infection and disease. In C57BL/6J mice, prior nasal administration of virulent B. pertussis BPSM and PT-deficient BPRA provided effective and sustained protection from IAV-induced mortality. However, BPSM or BPRA administered together with purified PT (BPRA + PT) had a stronger protective effect on weight loss compared to BPRA alone, reduced the viral load, and induced IL-17A in the lungs. In IL-17^-/- mice, BPSM- and BPRA + PT-mediated protection against viral replication was abolished, while BPSM, BPRA and BPRA + PT provided similar levels of protection against IAV-induced mortality and weight loss. In conclusion, B. pertussis infection protects against influenza by two mechanisms: one reducing viral replication depending on PT and IL-17, and the other, independently of PT and IL-17, resulting in protection against influenza disease without reducing the viral load.

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来源期刊

Microbes and Infection 医学-病毒学

CiteScore

12.60

自引率

1.70%

发文量

审稿时长

40 days

期刊介绍： Microbes and Infection publishes 10 peer-reviewed issues per year in all fields of infection and immunity, covering the different levels of host-microbe interactions, and in particular: the molecular biology and cell biology of the crosstalk between hosts (human and model organisms) and microbes (viruses, bacteria, parasites and fungi), including molecular virulence and evasion mechanisms. the immune response to infection, including pathogenesis and host susceptibility. emerging human infectious diseases. systems immunology. molecular epidemiology/genetics of host pathogen interactions. microbiota and host "interactions". vaccine development, including novel strategies and adjuvants. Clinical studies, accounts of clinical trials and biomarker studies in infectious diseases are within the scope of the journal. Microbes and Infection publishes articles on human pathogens or pathogens of model systems. However, articles on other microbes can be published if they contribute to our understanding of basic mechanisms of host-pathogen interactions. Purely descriptive and preliminary studies are discouraged.