BspR/BtrA, an Anti-σ Factor, Regulates the Ability of Bordetella bronchiseptica To Cause Cough in Rats
BspR/BtrA, an Anti-σ Factor, Regulates the Ability of Bordetella bronchiseptica To Cause Cough in Rats
复制标题
BspR/BtrA 是一种抗 σ 因子，可调节支气管败血博德特氏菌引起大鼠咳嗽的能力
DOI：
10.1128/msphere.00093-19
复制
发表时间：
2019
期刊：
影响因子：
4.8
通讯作者：
Horiguchi Yasuhiko
中科院分区：
文献类型：
--
作者：
Nakamura Keiji;Shinoda Noriko;Hiramatsu Yukihiro;Ohnishi Shinya;Kamitani Shigeki;Ogura Yoshitoshi;Hayashi Tetsuya;Horiguchi Yasuhiko
百日咳杆菌，B。副百日咳和B.支气管败血症引起呼吸道感染，其中许多以受感染宿主的咳嗽为特征。咳嗽的发病机制仍有待分析，这主要是因为没有方便的小动物感染模型复制博德特氏菌感染后咳嗽。在这里，我们提出了一个咳嗽模型的大鼠感染B。支气管炎大鼠是B的自然宿主之一。支气管败血症，很容易感染的有机体，并表现出频繁咳嗽。B。百日咳也引起大鼠咳嗽，这与以前的报道一致，但咳嗽反应不如B明显。支气管败血症引起的咳嗽通过使用大鼠模型，我们证明了腺苷酸环化酶毒素、皮肤坏死毒素和III型分泌系统不参与咳嗽产生，但BspR/BtrA（同一蛋白质的不同名称），一种抗σ因子，调节未知因子的产生以引起咳嗽。通过不仅接种活细菌而且接种细菌裂解物来观察大鼠咳嗽。感染bspR（btrA）缺陷型菌株引起的咳嗽频率明显低于野生型;然而，鼻内接种abspR（btrA）缺陷型菌株的裂解物引起的咳嗽与野生型相似，表明BspR/BtrA仅在细菌定殖宿主体内时调节咳嗽因子的产生。此外，发现咳嗽因子是热不稳定的并且由B产生。支气管败血症在Bvg+阶段。百日咳是由百日咳杆菌引起的一种呼吸道传染病，是一种急性呼吸道传染病。该病的特征是严重的阵发性咳嗽，这对患者来说是一个沉重的负担，偶尔会导致死亡;然而，其发病机制在很大程度上仍然未知。分析博德特氏菌引起的咳嗽的主要障碍是缺乏复制咳嗽的传统动物模型。由于百日咳博德特氏菌对人类高度适应，因此认为实验动物中的感染模型尚未充分建立。在本研究中，我们检查了感染B的大鼠的咳嗽。支气管败血症，它与B共享许多毒力因子。百日咳。利用该模型，我们证实了博德特氏菌的一些主要毒力因子不参与咳嗽的产生，而是参与B的抗σ因子BspR/BtrA。支气管败血症调节未知的引起咳嗽的细菌因子的产生。我们的研究结果为理解博德特氏菌引起咳嗽的机制提供了重要线索。
Bordetella pertussis, B. parapertussis, and B. bronchiseptica cause respiratory infections, many of which are characterized by coughing of the infected hosts. The pathogenesis of the coughing remains to be analyzed, mainly because there were no convenient infection models of small animals that replicate coughing afterBordetellainfection. Here, we present a coughing model of rats infected with B. bronchiseptica. Rats, which are one of natural hosts of B. bronchiseptica, were readily infected with the organisms and showed frequent coughing. B. pertussis also caused coughing in rats, which is consistent with previous reports, but the cough response was less apparent than the B. bronchiseptica-induced cough. By using the rat model, we demonstrated that adenylate cyclase toxin, dermonecrotic toxin, and the type III secretion system are not involved in cough production, but BspR/BtrA (different names for the same protein), an anti-σ factor, regulates the production of unknown factor(s) to cause coughing. Rat coughing was observed by inoculation of not only the living bacteria but also the bacterial lysates. Infection withbspR(btrA)-deficient strains caused significantly less frequent coughing than the wild type; however, intranasal inoculation of the lysates from abspR(btrA)-deficient strain caused coughing similarly to the wild type, suggesting that BspR/BtrA regulates the production of the cough factor(s) only when the bacteria colonize host bodies. Moreover, the cough factor(s) was found to be heat labile and produced by B. bronchiseptica in the Bvg+phase. We consider that our rat model provides insight into the pathogenesis of cough induced by theBordetellainfection.IMPORTANCEWhooping cough is a contagious respiratory disease caused by Bordetella pertussis. This disease is characterized by severe paroxysmal coughing, which becomes a heavy burden for patients and occasionally results in death; however, its pathogenesis remains largely unknown. The major obstacle to analyzingBordetella-induced coughing is the lack of conventional animal models that replicate coughing. As Bordetella pertussis is highly adapted to humans, infection models in experimental animals are not considered to be well established. In the present study, we examined coughing in rats infected with B. bronchiseptica, which shares many virulence factors with B. pertussis. Using this rat model, we demonstrated that some of the major virulence factors ofBordetellaare not involved in cough production, but an anti-σ factor, BspR/BtrA, of B. bronchiseptica regulates the production of unknown cough-causing bacterial factor(s). Our results provide important clues to understand the mechanism by whichBordetellainduces cough.
登录
查看更多内容
DOI：
10.1099/00221287-63-2-211
发表时间：
1970-01-01
期刊：
JOURNAL OF GENERAL MICROBIOLOGY
影响因子：
--
作者：
STAINER, DW;SCHOLTE, MJ
通讯作者：
SCHOLTE, MJ
影响因子：
3
作者：
HALL, E;PARTON, R;WARDLAW, AC
通讯作者：
WARDLAW, AC
DOI：
10.1073/pnas.120163297
发表时间：
2000-06-06
影响因子：
11.1
作者：
Datsenko, KA;Wanner, BL
通讯作者：
Wanner, BL
影响因子：
3.6
作者：
Julio SM;Inatsuka CS;Mazar J;Dieterich C;Relman DA;Cotter PA
通讯作者：
Cotter PA
影响因子：
3.3
作者：
Hornibrook, J. W.;Ashburn, L. L.
通讯作者：
Ashburn, L. L.