Abstract
More than 80% of infectious bacteria form biofilm, which is a bacterial cell community surrounded by secreted polysaccharides, proteins and glycolipids. Such bacterial superstructure increases resistance to antimicrobials and host defenses. Thus, to control these biofilm-forming pathogenic bacteria requires antimicrobial agents with novel mechanisms or properties. Pseudomonas aeruginosa, a Gram-negative opportunistic nosocomial pathogen, is a model strain to study biofilm development and correlation between biofilm formation and infection. In this study, a recombinant hemolymph plasma lectin (rHPLOE) cloned from Taiwanese Tachypleus tridentatus was expressed in an Escherichia coli system. This rHPLOE was shown to have the following properties: (1) Binding to P. aeruginosa PA14 biofilm through a unique molecular interaction with rhamnose-containing moieties on bacteria, leading to reduction of extracellular di-rhamnolipid (a biofilm regulator); (2) decreasing downstream quorum sensing factors, and inhibiting biofilm formation; (3) dispersing the mature biofilm of P. aeruginosa PA14 to improve the efficacies of antibiotics; (4) reducing P. aeruginosa PA14 cytotoxicity to human lung epithelial cells in vitro and (5) inhibiting P. aeruginosa PA14 infection of zebrafish embryos in vivo. Taken together, rHPLOE serves as an anti-biofilm agent with a novel mechanism of recognizing rhamnose moieties in lipopolysaccharides, di-rhamnolipid and structural polysaccharides (Psl) in biofilms. Thus rHPLOE links glycan-recognition to novel anti-biofilm strategies against pathogenic bacteria.
Highlights
Part of the reasons for bacterial resistance to antibiotics are due to the formation of biofilm, composed of secreted polysaccharides, proteins, glycolipids and small molecules in the bacterial microenvironment
The addition of 100 Mm of d-mannose, d-glucose, d-fructose, d-galactose and alginate could not reduce the binding between rHPLOE and the extracted biofilm. These results indicated that rHPLOE bound to rhamnose containing components in P. aeruginosa
RHPLDM did not disperse the mature biofilm. These results indicated that rHPLOE inhibited biofilm formation and dispersed the mature biofilm of P. aeruginosa PA14 and that both activities perhaps are correlated with the rhamnose binding activity
Summary
Part of the reasons for bacterial resistance to antibiotics are due to the formation of biofilm, composed of secreted polysaccharides, proteins, glycolipids and small molecules in the bacterial microenvironment. Mar. Drugs 2019, 17, 355 formation by non-microbicidal mechanisms is an example of anti-pathogenic approaches [2,3]. Pseudomonas aeruginosa, is responsible for various infections, in immuno-compromised individuals [4], and it forms biofilms to make antibiotic treatments inefficient and promotes acute infections, for example, at upper airway, skin, wound, urinary tract, enteric and lung [5]. The PA14 islands carried several genes implicated in virulence that are absent in PAO1, including genes encoding effectors of the type III secretion system for secreting virulent factors [7,8].
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