Effect of Alginate Lyase on Biofilm-GrownHelicobacter pyloriProbed by Atomic Force Microscopy

Alessandro Maiorana,Margherita Cacaci,Valentina Palmieri,Francesca Bugli,Riccardo Torelli,Gabriele Ciasca,Giuseppe Maulucci,Brunella Posteraro,Marco De Spirito,Massimiliano Papi,Maurizio Sanguinetti,Francesco Paroni Sterbini

doi:10.1155/2015/989516

Alessandro Maiorana, Margherita Cacaci + Show 10 more

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https://doi.org/10.1155/2015/989516

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Abstract

Helicobacter pylori(H. pylori) is a microorganism with a pronounced capability of adaptation under environmental stress solicitations. Its persistence and antimicrobial resistance to the drugs commonly used in the anti-H. pyloritherapy are associated with the development of a biofilm mainly composed of DNA, proteins, and polysaccharides. A fundamental step to increase the success of clinical treatments is the development of new strategies and molecules able to interfere with the biofilm architecture and thus able to enhance the effects of antibiotics. By using Atomic Force Microscopy and Scanning Electron Microscopy we analyzed the effects of the alginate lyase (AlgL), an enzyme able to degrade a wide class of polysaccharides, on theH. pylorishape, surface morphology, and biofilm adhesion properties. We demonstrated that AlgL generates a noticeable loss ofH. pyloricoccoid form in favor of the bacillary form and reduces theH. pyloriextracellular polymeric substances (EPS).

Highlights

Helicobacter pylori is one of the causative agents of gastritis and peptic ulcer diseases and is considered as a risk factor for gastric carcinoma [1, 2]
A fundamental step to increase the success of clinical treatments is the development of new strategies and molecules able to interfere with the biofilm architecture and able to enhance the effects of antibiotics
We demonstrated that alginate lyase (AlgL) generates a noticeable loss of H. pylori coccoid form in favor of the bacillary form and reduces the H. pylori extracellular polymeric substances (EPS)

Summary

Introduction

Helicobacter pylori is one of the causative agents of gastritis and peptic ulcer diseases and is considered as a risk factor for gastric carcinoma [1, 2]. Helicobacter pylori is a microorganism with a pronounced capability of adaptation under environmental stress solicitations [3]. Helicobacter pylori is capable of forming a mature biofilm characterized by clustered bacterial cells arranged in an abundant matrix after 3 days of incubation in vitro [9,10,11]. Cell aggregation and early adhesion to surfaces are both dependent on the properties of the bacterium surface that is modulated by the composition of the extracellular matrix. H. pylori is able to modulate its shape from bacillary form to coccoid form to fit the environmental conditions and its virulence is strongly dependent on its cellular morphology. It is regarded that the bacillary H. pylori transforms to the coccoid form under stressfully environmental conditions [15,16,17,18]. Transformation into the coccoid form is an active, biologically led process, switched on by the bacterium as a protection mechanism

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