University of Maryland School of Medicine, Baltimore, Maryland, USA.
mBio. 2022 Jun 28;13(3):e0091722. doi: 10.1128/mbio.00917-22. Epub 2022 May 23.
What causes the cough in whooping cough (pertussis) has been a longstanding question in the field but has been difficult to answer because of the perceived lack of convenient small animal models. Y. Hiramatsu, K. Suzuki, T. Nishida, N. Onoda, et al. (mBio 13:e01397-21, 2022, https://doi.org/10.1128/mbio.03197-21) used a mouse model and cellular studies to investigate bacterial and host factors that contribute to cough production during Bordetella pertussis infection. In elegant studies, they found that the bacterial factors pertussis toxin, lipooligosaccharide, and Vag8 function cooperatively to produce cough. These factors induce production of host bradykinin, a known cough inducer that sensitizes the ion channel TRPV1 on neurons, and they investigated host signaling pathways altered by the bacterial factors that exacerbate cough responses. This is a highly significant and important finding that not only elucidates mechanisms underlying the pathophysiology of the severe cough, but also may reveal potential novel therapeutic approaches to treat individuals suffering from the debilitating effects of cough in pertussis.
百日咳(百日咳)的咳嗽原因一直是该领域的一个长期存在的问题,但由于缺乏方便的小动物模型,因此很难回答这个问题。Y. Hiramatsu、K. Suzuki、T. Nishida、N. Onoda 等人(mBio 13:e01397-21,2022,https://doi.org/10.1128/mbio.03197-21)使用小鼠模型和细胞研究来调查导致百日咳博德特氏菌感染期间咳嗽产生的细菌和宿主因素。在一项精巧的研究中,他们发现细菌因子百日咳毒素、脂寡糖和 Vag8 协同作用产生咳嗽。这些因子诱导宿主缓激肽的产生,缓激肽是一种已知的咳嗽诱导剂,可使神经元上的离子通道 TRPV1 敏化,它们还研究了细菌因子改变的宿主信号通路,这些信号通路加剧了咳嗽反应。这是一个非常重要和重要的发现,不仅阐明了严重咳嗽的病理生理学的机制,而且还可能揭示出治疗因百日咳而遭受咳嗽衰弱影响的个体的潜在新治疗方法。