Department of Microbiology and Immunology, Wake Forest University Health Sciences, Winston-Salem, North Carolina, USA.
mBio. 2010 Jul 6;1(3):e00102-10. doi: 10.1128/mBio.00102-10.
Otitis media (OM) is among the leading diseases of childhood and is caused by opportunists that reside within the nasopharynx, such as Haemophilus influenzae and Moraxella catarrhalis. As with most airway infections, it is now clear that OM infections involve multiple organisms. This study addresses the hypothesis that polymicrobial infection alters the course, severity, and/or treatability of OM disease. The results clearly show that coinfection with H. influenzae and M. catarrhalis promotes the increased resistance of biofilms to antibiotics and host clearance. Using H. influenzae mutants with known biofilm defects, these phenotypes were shown to relate to biofilm maturation and autoinducer-2 (AI-2) quorum signaling. In support of the latter mechanism, chemically synthesized AI-2 (dihydroxypentanedione [DPD]) promoted increased M. catarrhalis biofilm formation and resistance to antibiotics. In the chinchilla infection model of OM, polymicrobial infection promoted M. catarrhalis persistence beyond the levels seen in animals infected with M. catarrhalis alone. Notably, no such enhancement of M. catarrhalis persistence was observed in animals infected with M. catarrhalis and a quorum signaling-deficient H. influenzae luxS mutant strain. We thus conclude that H. influenzae promotes M. catarrhalis persistence within polymicrobial biofilms via interspecies quorum signaling. AI-2 may therefore represent an ideal target for disruption of chronic polymicrobial infections. Moreover, these results strongly imply that successful vaccination against the unencapsulated H. influenzae strains that cause airway infections may also significantly impact chronic M. catarrhalis disease by removing a reservoir of the AI-2 signal that promotes M. catarrhalis persistence within biofilm.
中耳炎(OM)是儿童期的主要疾病之一,由居住在鼻咽部的机会致病菌引起,如流感嗜血杆菌和卡他莫拉菌。与大多数气道感染一样,现在很清楚,OM 感染涉及多种生物体。本研究旨在验证以下假说,即混合感染会改变 OM 疾病的病程、严重程度和/或可治疗性。研究结果清楚地表明,流感嗜血杆菌和卡他莫拉菌的共感染会增加生物膜对抗生素和宿主清除的抵抗力。使用具有已知生物膜缺陷的流感嗜血杆菌突变体,这些表型与生物膜成熟和自诱导物-2(AI-2)群体信号有关。为了支持后一种机制,用化学合成的 AI-2(二羟戊二酮[DPD])促进了卡他莫拉菌生物膜形成和对抗生素的抵抗力的增加。在 OM 的豚鼠感染模型中,混合感染促进了卡他莫拉菌的持续存在,超过了单独感染卡他莫拉菌的动物中观察到的水平。值得注意的是,在感染卡他莫拉菌和缺乏群体信号的流感嗜血杆菌 luxS 突变株的动物中,没有观察到卡他莫拉菌持续存在的增强。因此,我们得出结论,流感嗜血杆菌通过种间群体信号促进了生物膜中卡他莫拉菌的持续存在。AI-2 可能因此代表了破坏慢性多微生物感染的理想靶点。此外,这些结果强烈暗示,针对引起气道感染的无荚膜流感嗜血杆菌菌株的成功疫苗接种也可能通过消除促进生物膜中卡他莫拉菌持续存在的 AI-2 信号的储库,显著影响慢性卡他莫拉菌病。