Department of Otorhinolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Japan.
Department of Ophthalmology, Wakayama Medical University, Wakayama, Japan.
Infect Immun. 2024 Oct 15;92(10):e0014624. doi: 10.1128/iai.00146-24. Epub 2024 Aug 7.
Transmission is the first step for a microorganism to establish colonization in the respiratory tract and subsequent development of infectious disease. is a leading pathogen that colonizes the mucosal surfaces of the human upper respiratory tract and causes subsequent transmission and invasive infections especially in co-infection with influenza A virus. Host factors contributing to respiratory contagion are poorly understood. Transient receptor potential vanilloid (TRPV) channels have various roles in response to microoorganism. Inhibition of TRPV exacerbates invasive infection by , but it is unclear how TRPV channels influence pneumococcal transmission. Here, we describe the effect of inhibition of TRPV1 on pneumococcal transmission. We adopted a TRPV1-deficient infant mouse model of pneumococcal transmission during co-infection with influenza A virus. We also analyzed the expression of nasal mucin or pro-inflammatory cytokines. TRPV1 deficiency attenuated pneumococcal transmission and shedding during co-infection with influenza A virus. TRPV1 deficiency suppressed the expression of nasal mucin. In addition, there were increases in the expression of tumor necrosis factor-α and type I interferon, followed by the suppressed replication of influenza A virus in TRPV1-deficient mice. Inhibition of TRPV1 was shown to attenuate pneumococcal transmission by reducing shedding through the suppression of nasal mucin during co-infection with influenza A virus. Inhibition of TRPV1 suppressed nasal mucin by modulation of pro-inflammatory responses and regulation of replication of influenza A virus. TRPV1 could be a new target in preventive strategy against pneumococcal transmission.
传播是微生物在呼吸道建立定植并随后发展为传染病的第一步。肺炎链球菌是一种主要病原体，定植于人类上呼吸道的黏膜表面，导致随后的传播和侵袭性感染，特别是在与甲型流感病毒共同感染时。宿主因素导致呼吸道传染的机制尚未完全阐明。瞬时受体电位香草酸 (TRPV) 通道在微生物反应中具有多种作用。TRPV 通道的抑制会加重肺炎链球菌的侵袭性感染，但尚不清楚 TRPV 通道如何影响肺炎球菌的传播。在这里，我们描述了抑制 TRPV1 对肺炎球菌传播的影响。我们采用了 TRPV1 缺陷的婴儿肺炎链球菌传播模型，该模型在感染甲型流感病毒时存在共感染。我们还分析了鼻黏液或促炎细胞因子的表达。TRPV1 缺陷减弱了甲型流感病毒共感染期间的肺炎球菌传播和脱落。TRPV1 缺陷抑制了鼻黏液的表达。此外，肿瘤坏死因子-α和 I 型干扰素的表达增加，随后甲型流感病毒在 TRPV1 缺陷小鼠中的复制受到抑制。抑制 TRPV1 通过抑制鼻黏液减少脱落来减轻甲型流感病毒共感染期间的肺炎球菌传播。TRPV1 通过调节促炎反应和调节甲型流感病毒的复制来抑制鼻黏液。TRPV1 可能成为预防肺炎球菌传播的新靶点。
