Title Extracellular products-mediated interspecific interaction between Pseudomonas aeruginosa and Escherichia coli
Author Yang Yuan1, Jing Li1, Jiafu Lin1, Wenjuan Pan1, Yiwen Chu1, Balakrishnan Prithiviraj2, Yidong Guo1, Xinrong Wang1*, and Kelei Zhao1*
Address 1Antibiotics Research and Re-evaluation Key Laboratory of Sichuan Province, Sichuan Industrial Institute of Antibiotics, Chengdu University, Chengdu 610052, Sichuan, P. R. China, 2Marine Bio-products Research Laboratory, Department of Plant, Food and Environmental Sciences, Dalhousie University, Truro B2N 5E3, NS, Canada
Bibliography Journal of Microbiology, 59(1),29–40, 2021,
DOI 10.1007/s12275-021-0478-0
Key Words Pseudomonas aeruginosa, Escherichia coli, interaction, transcriptional profile, pyocyanin, virulence
Abstract The Gram-negative pathogen Pseudomonas aeruginosa adopts several elaborate strategies to colonize a wide range of natural or clinical niches and to overcome the neighboring bacterial competitors in polymicrobial communities. However, the relationship and interaction mechanism of P. aeruginosa with other bacterial pathogens remains largely unexplored. Here we explore the interaction dynamics of P. aeruginosa and Escherichia coli, which frequently coinfect the lungs of immunocompromised hosts, by using a series of on-plate proximity assays and RNA-sequencing. We show that the extracellular products of P. aeruginosa can inhibit the growth of neighboring E. coli and induce a large-scale of transcriptional reprogramming of E. coli, especially in terms of cellular respiration- related primary metabolisms and membrane components. In contrast, the presence of E. coli has no significant effect on the growth of P. aeruginosa in short-term culture, but causes a dysregulated expression of genes positively controlled by the quorum-sensing (QS) system of P. aeruginosa during subsequent pairwise culture. We further demonstrate that the divergent QS-regulation of P. aeruginosa may be related to the function of the transcriptional regulator PqsR, which can be enhanced by E. coli culture supernatant to increase the pyocyanin production by P. aeruginosa in the absence of the central las-QS system. Moreover, the extracellular products of E. coli promote the proliferation and lethality of P. aeruginosa in infecting the Caenorhabditis elegans model. The current study provides a general characterization of the extracellular products-mediated interactions between P. aeruginosa and E. coli, and may facilitate the understanding of polymicrobial infections.