Abstract

Pseudomonas aeruginosa is an opportunistic pathogen often involved in airway infections of cystic fibrosis (CF) patients. Its pathogenicity is related to several virulence factors, such as biofilm formation, motility and production of toxins and proteases. The expression of these virulence factors is controlled by quorum sensing (QS). Thus, QS inhibition is considered a novel strategy for the development of antipathogenic compounds acting on specific bacterial virulence programs without affecting bacterial vitality. In this context, cold-adapted marine bacteria living in polar regions represent an untapped reservoir of biodiversity endowed with an interesting chemical repertoire. In this paper, we investigated the biological activity of a supernatant derived from a novel Antarctic bacterium (SN_TAE2020) against specific virulence factors produced by P. aeruginosa strains isolated from FC patients. Our results clearly show a reduction in pyocyanin and protease production in the presence of SN_TAE2020. Finally, SN_TAE2020 was also able to strongly affect swarming and swimming motility for almost all tested strains. Furthermore, the effect of SN_TAE2020 was investigated on biofilm growth and texture, captured by SEM analysis. In consideration of the novel results obtained on clinical strains, polar bacteria might represent potential candidates for the discovery of new compounds limiting P. aeruginosa virulence in CF patients.

Highlights

  • The selection of P. aeruginosa isolates was based on specific virulence factors, such as pyocyanin production, proteolytic activity, biofilm formation and swarming and swimming motility

  • [28], to investigate its capability to impair formation, protease swarming and the results show that it did notFirst, affectwe bacterial at all tested motility and pyocyanin production

  • Mainly during chronic infections, such those occurring in the lungs of aeruginosa can acquire new resistance as those occurring in the lungs of cystic fibrosis (CF) patients, P. aeruginosa can acquire new remechanisms via horizontal gene transfer sistance mechanisms via horizontal gene[24]

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Summary

Introduction

Cystic fibrosis (CF) is a progressive genetic disease caused by the presence of mutations in the cftr gene, encoding for a protein called cystic fibrosis transmembrane conductance regulator (CFTR). This mutation has been reported to alter the transport across the cellular membrane, especially in the airways [1]. A defective CFTR protein produces thick, sticky mucus that clogs the airways, trapping microorganisms, leading to inflammation and recurrent and chronic infections, which cause respiratory failure and other complications [2]. Starting from childhood, Staphylococcus aureus (S. aureus) is one of the first colonizers of the CF airways, followed by Haemophilus influenzae (H. influenzae) and during adolescence and for all patient life, the opportunistic pathogen Pseudomonas aeruginosa

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