Abstract
Pseudomonas aeruginosa is an opportunistic pathogen that causes severe infections, such as pneumonia and bacteremia. Several studies demonstrated that flagellar motility is an important virulence factor for P. aeruginosa infection. In this study, we determined whether sulfated vizantin affects P. aeruginosa flagellar motility in the absence of direct antimicrobial activity. We found that 100 μM sulfated vizantin suppressed P. aeruginosa PAO1 from penetrating through an artificial mucin layer by affecting flagellar motility, although it did not influence growth nor bacterial protease activity. To further clarify the mechanism in which sulfated vizantin suppresses the flagellar motility of P. aeruginosa PAO1, we examined the effects of sulfated vizantin on the composition of the flagellar filament and mRNA expression of several flagella-related genes, finding that sulfated vizantin did not influence the composition of the flagellar complex (fliC, motA, and motB) in P. aeruginosa PAO1, but significantly decreased mRNA expression of the chemotaxis-related genes cheR1, cheW, and cheZ. These results indicated that sulfated vizantin is an effective inhibitor of flagellar motility in P. aeruginosa.
Highlights
Pseudomonas aeruginosa is an opportunistic pathogen that causes severe pneumonia and bacteremia, which are associated with high mortality [1, 2]
We examined whether sulfated vizantin inhibited the flagellar motility of P. aeruginosa PAO1
Our results demonstrated that sulfated vizantin suppressed penetration of P. aeruginosa PAO1 through an artificial mucin layer and inhibited swimming motility without influencing the growth rate of P. aeruginosa PAO1 or influencing protease activity
Summary
Pseudomonas aeruginosa is an opportunistic pathogen that causes severe pneumonia and bacteremia, which are associated with high mortality [1, 2]. Colonization with P. aeruginosa occurs in critical body organs, such as the lung [3], urinary tract [4], and intestine [5], with potentially fatal results. Numerous microorganisms can penetrate mucous layers using motility and enzymes that degrade mucins in order to reach host epithelial-cell surfaces [6, 7]. P. aeruginosa can subvert mucin layers and reach the surface of host epithelial cells [8]. P. aeruginosa utilizes many kinds of virulence factors, including flagella, type IV pili, types II, III, and VI effectors, biofilm, proteases, and lipopolysaccharides [9,10,11].
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