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发病机制可能是铜绿假单胞菌社会的一种反作弊机制。

Pathogenesis could be one of the anti-cheating mechanisms for Pseudomonas aeruginosa society.

机构信息

Department of Endodontics, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, PR China.

出版信息

Med Hypotheses. 2011 Feb;76(2):166-8. doi: 10.1016/j.mehy.2010.09.007. Epub 2010 Oct 8.

DOI:10.1016/j.mehy.2010.09.007
PMID:20934258
Abstract

Pseudomonas aeruginosa is the major pathogen of chronic lung infections in individuals with cystic fibrosis (CF). Traditionally, it has been regarded as living in planktonic form, and as being able to perform only simple physiological activities. Recent studies in biofilm infections in CF patients, however, show that P. aeruginosa can perform many social behaviors, like cooperation and cheating. Based on the theory of "survival of the fittest", it may be presumed that every individual will take advantage of cheating instead of cooperation to increase its fitness, at the cost of group survival. In reality, however, a bacterial society can remain stable, even though cheaters arise frequently in the population. It is therefore possible that there are anti-cheating mechanisms in a bacterial society. The cheaters of P. aeruginosa will cause the loss or the decrease of the pathogenesis of the microorganism in the cystic fibrosis host. These defects in pathogenesis will be disadvantageous to bacterial colonization and compromise the resistance to host immunity. We therefore propose the hypothesis that the pathogenesis in cystic fibrosis lung infections could be one of the anti-cheating mechanisms that contribute to the hidden costs of the cheater strains. To test this hypothesis, we designed an experiment in an animal model of CF. If this hypothesis can be confirmed, it will illustrate that nontrivial analogies exist between microbial social behaviors and the social traits that are observed in the more traditional model systems for sociobiology. This will not only provide a genetic model for sociobiology research, but also cast light on the social control of chronic bacterial infections.

摘要

铜绿假单胞菌是囊性纤维化(CF)患者慢性肺部感染的主要病原体。传统上,它被认为以浮游形式存在,只能进行简单的生理活动。然而,最近对 CF 患者生物膜感染的研究表明,铜绿假单胞菌可以表现出许多社会行为,如合作和欺骗。基于“适者生存”的理论,可以推测每个个体都会利用欺骗而不是合作来增加其适应性,而牺牲群体的生存。然而,在现实中,即使群体中经常出现骗子,细菌社会也可以保持稳定。因此,细菌社会中可能存在反欺骗机制。铜绿假单胞菌的骗子会导致微生物在囊性纤维化宿主中的致病性丧失或减少。这些致病性的缺陷对细菌定植不利,并损害对宿主免疫的抵抗力。因此,我们提出假设,即囊性纤维化肺部感染的发病机制可能是导致骗子菌株隐藏代价的反欺骗机制之一。为了验证这一假设,我们在 CF 动物模型中设计了一项实验。如果这一假设能够得到证实,它将说明微生物社会行为与社会生物学中更传统的模型系统中观察到的社会特征之间存在着重要的类比。这不仅为社会生物学研究提供了一个遗传模型,也为慢性细菌感染的社会控制提供了启示。

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Pathogenesis could be one of the anti-cheating mechanisms for Pseudomonas aeruginosa society.发病机制可能是铜绿假单胞菌社会的一种反作弊机制。
Med Hypotheses. 2011 Feb;76(2):166-8. doi: 10.1016/j.mehy.2010.09.007. Epub 2010 Oct 8.
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Infections with Pseudomonas aeruginosa in patients with cystic fibrosis.囊性纤维化患者的铜绿假单胞菌感染
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[Investigation of biofilm formation and relationship with genotype and antibiotic susceptibility of Pseudomonas aeruginosa strains isolated from patients with cystic fibrosis].[囊性纤维化患者分离出的铜绿假单胞菌菌株生物膜形成及其与基因型和抗生素敏感性关系的研究]
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Emergence and persistence of Pseudomonas aeruginosa in the cystic fibrosis airway.铜绿假单胞菌在囊性纤维化气道中的出现与持续存在。
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