Attenuation of Edwardsiella tarda Virulence by Small Peptides That Interfere with LuxS/Autoinducer Type 2 Quorum Sensing

Edwardsiella tarda is a gram-negative pathogen with a broad host range that includes humans, animals, and fish. Recent studies have shown that the LuxS/autoinducer type 2 (AI-2) quorum sensing system is involved in the virulence of E. tarda. In the present study, it was found that the E. tarda LuxS mutants bearing deletions of the catalytic site (C site) and the tyrosine kinase phosphorylation site, respectively, are functionally inactive and that these dysfunctional mutants can interfere with the activity of the wild-type LuxS. Two small peptides, 5411 and 5906, which share sequence identities with the C site of LuxS, were identified. 5411 and 5906 proved to be inhibitors of AI-2 activity and could vitiate the infectivity of the pathogenic E. tarda strain TX1. The inhibitory effect of 5411 and 5906 on AI-2 activity is exerted on LuxS, with which these peptides specifically interact. The expression of 5411 and 5906 in TX1 has multiple effects (altering biofilm production and the expression of certain virulence-associated genes), which are similar to those caused by interruption of luxS expression. Further study found that it is very likely that 5411 and 5906 can be released from the strains expressing them and, should TX1 be in the vicinity, captured by TX1. Based on this observation, a constitutive 5411 producer (Pseudomonas sp. strain FP3/pT5411) was constructed in the form of a fish commensal isolate that expresses 5411 from a plasmid source. The presence of FP3/pT5411 in fish attenuates the virulence of TX1. Finally, it was demonstrated that fish expressing 5411 directly from tissues exhibit enhanced resistance against TX1 infection.

Attenuation of Edwardsiella tarda Virulence by Small Peptides That Interfere with LuxS/Autoinducer Type 2 Quorum Sensing

Edwardsiella tarda is a gram-negative pathogen with a broad host range that includes humans, animals, and fish. Recent studies have shown that the LuxS/autoinducer type 2 (AI-2) quorum sensing system is involved in the virulence of E. tarda. In the present study, it was found that the E. tarda LuxS mutants bearing deletions of the catalytic site (C site) and the tyrosine kinase phosphorylation site, respectively, are functionally inactive and that these dysfunctional mutants can interfere with the activity of the wild-type LuxS. Two small peptides, 5411 and 5906, which share sequence identities with the C site of LuxS, were identified. 5411 and 5906 proved to be inhibitors of AI-2 activity and could vitiate the infectivity of the pathogenic E. tarda strain TX1. The inhibitory effect of 5411 and 5906 on AI-2 activity is exerted on LuxS, with which these peptides specifically interact. The expression of 5411 and 5906 in TX1 has multiple effects (altering biofilm production and the expression of certain virulence-associated genes), which are similar to those caused by interruption of luxS expression. Further study found that it is very likely that 5411 and 5906 can be released from the strains expressing them and, should TX1 be in the vicinity, captured by TX1. Based on this observation, a constitutive 5411 producer (Pseudomonas sp. strain FP3/pT5411) was constructed in the form of a fish commensal isolate that expresses 5411 from a plasmid source. The presence of FP3/pT5411 in fish attenuates the virulence of TX1. Finally, it was demonstrated that fish expressing 5411 directly from tissues exhibit enhanced resistance against TX1 infection.

金融工作者的抑郁症状的影响因素及其形成机制研究

Ill-health prevails in the workplace. A key problem encountered in the area of stress management is a lack of research into the way job burnout turns into mental problems, especially depressive symptoms, the most prevalent and costly psychiatric condition in the workplace. This research belongs to a cross-discipline area of industrial psychiatry and organizational behavior, which has seldom been investigated before. This research will contribute to the theoretical development of organizational behavior, especially to stress management and industrial psychiatry. This study aims to explore etiological factors and mechanisms of depressive symptoms of workers in the financial industry. By using literature review, semi-structured interviews and surveys as the major research methods, this Ph.D. study systematically investigated the risk factors of workers’ depressive symptoms within and outside of the work area. These risk factors are worker-work environment fits, work family conflicts, and workers’ psychological vulnerabilities to depression. A thorough literature review and 20 semi-structured interviews of brokers in different kinds of financial markets show the feasibility and necessity of this Ph.D. study when it comes to the issue of financial workers’ depressive symptoms. Two surveys of workplace-etiological factors of depressive symptoms were conducted among 244 financial workers and 1024 financial workers. This cross-sample verification showed that worker-work environment fit was a good framework to study risk factors of workers’ depressive symptoms. Results revealed that job demands-abilities misfit could lead to job burnout which in turn contributed to worker’s depressive symptoms; besides this, work effort-reward imbalance could directly cause workers’ depressive symptoms. Emotional labor enhanced the positive effect of job burnout on workers’ depressive symptoms. In the third study, a prominent risk factor outside of the work area, namely work family conflict, and workers’ psychological vulnerabilities of depression were included with workplace etiological factors to investigate the overall predictive model of depressive symptoms of financial workers. The survey was conducted among the same 1024 financial workers. Results indicated that work effort-reward imbalance, job burnout and work interfering in family life were three external etiological factors of workers’ depressive symptoms. Neuroticism, autonomy and low emotional intelligence were three individual etiological factors which had a positive effect on workers’ depressive symptoms. Moreover, neuroticism enhanced the relationship between job burnout and depressive symptoms as well as between work interfering in family life and depressive symptoms. Autonomy aggravated the relationship between job burnout and depressive symptoms. However, emotional intelligence attenuated the relationship between job burnout and depressive symptoms as well as between work effort-reward imbalance and depressive symptoms. Besides, workers’ dysfunctional attitudes played a partial mediating role in the relationships between above etiological factors and depressive symptoms. In the same sample, research evidence of impairments of workers’ depressive symptoms to their work-life quality was also obtained. Specifically, depressive symptoms could predict workers’ presenteeism, absenteeism and turnover intention. Their subjective well-being was also lowered when suffering more severe depressive symptoms. This research provides a theoretical basis to management practices targeted to set up the Employee Assistance Program or even more specilised rehabilitation programs for workers with depressive symptoms so as to improve their work-life quality and and establish a harmonious enterprise.