BackgroundHelicobacter pylori forms biofilms on glass surfaces at the air-liquid interface in in vitro batch cultures; however, biofilms of H. pylori have not been well characterized. In the present study, we analyzed the ability of H. pylori strains to form biofilms and characterized the underlying mechanisms of H. pylori biofilm formation.ResultsStrain TK1402 showed strong biofilm forming ability relative to the other strains in Brucella broth supplemented with 7% FCS. The strong biofilm forming ability of TK1402 is reflected the relative thickness of the biofilms. In addition, outer membrane vesicles (OMV) were detected within the matrix of only the TK1402 biofilms. Biofilm formation was strongly correlated with the production of OMV in this strain. We further observed that strain TK1402 did not form thick biofilms in Brucella broth supplemented with 0.2% β-cyclodextrin. However, the addition of the OMV-fraction collected from TK1402 could enhance biofilm formation.ConclusionThe results suggested that OMV produced from TK1402 play an important role in biofilm formation in strain TK1402.
A dipeptide lantibiotic, named Smb, in Streptococcus mutans GS5 was characterized by molecular genetic approaches. The Smb biosynthesis gene locus is encoded by a 9.5-kb region of chromosomal DNA and consists of seven genes in the order smbM1, -T, -F, -M2, -G, -A, -B. This operon is not present in some other strains of S. mutans, including strain UA159. The genes encoding Smb were identified as smbA and smbB. Inactivation of smbM1, smbA, or smbB attenuated the inhibition of the growth of the indicator strain RP66, confirming an essential role for these genes in Smb expression. Mature Smb likely consists of the 30-amino-acid SmbA together with the 32-amino-acid SmbB. SmbA exhibited similarity with the mature lantibiotic lacticinA2 from Lactococcus lactis, while SmbB was similar to the mersacidin-like peptides from Bacillus halodurans and L. lactis. We also demonstrated that Smb expression is induced by the competence-stimulating peptide (CSP) and that a com box-like sequence is located in the smb promoter region. These results suggest that Smb belongs to the class I bacteriocin family, and its expression is dependent on CSP-induced quorum sensing.Dental caries has plagued humans since the dawn of civilization and still constitutes one of the most common human infectious diseases. Multiple species of bacteria inhabit the human oral cavity, and the species most commonly associated with human caries is Streptococcus mutans (22). Among the attributes thought to contribute to the virulence of S. mutans is its ability to elaborate antimicrobial or bacteriocin-like substances, which may provide a selective advantage for initial or sustained colonization in a milieu of densely packed competing organisms found in dental plaque (38,48).Bacteriocins are a family of ribosomally synthesized peptide antibiotics that are produced by bacteria (11,14,18,37 ). They are subdivided into four different classes based on biochemical and genetic characteristics (14,16,17). Class I and class II bacteriocins are by far the most extensively studied because they are the most abundant and most prominent in industrial applications (26). Class I bacteriocins, named lantibiotics, contain two modified amino acid residues, lanthionine and/or methyllanthionins, which are formed posttranslationally (7). The primary product of the lantibiotic structural gene is a precursor with an N-terminal leader sequence followed by a C-terminal propeptide which undergoes modification. Once modified within the cell, the bacteriocin is secreted by a dedicated transporter and the N-terminal leader sequence is cleaved by a protease (12, 49).Some strains of S. mutans produce antimicrobial substances called mutacins (3,4,30,34,35,36). Mutacins have been classified into two families: the lantibiotics and the nonlantibiotics. Classification of mutacin-producing strains based on their bactericidal activities, their sensitivities to other or selfproduced mutacins, and the presence of plasmids divides the mutacins into four types, I, II, III, and IV (28,34,35,36). Mutacins...
Bacterial biofilms are communities of microorganisms attached to a surface. Biofilm formation is critical not only for environmental survival but also for successful infection. Helicobacter pylori is one of the most common causes of bacterial infection in humans. Some studies demonstrated that this microorganism has biofilm forming ability in the environment and on human gastric mucosa epithelium as well as on in vitro abiotic surfaces. In the environment, H. pylori could be embedded in drinking water biofilms through water distribution system in developed and developing countries so that the drinking water may serve as a reservoir for H. pylori infection. In the human stomach, H. pylori forms biofilms on the surface of gastric mucosa, suggesting one possible explanation for eradication therapy failure. Finally, based on the results of in vitro analyses, H. pylori biofilm formation can decrease susceptibility to antibiotics and H. pylori antibiotic resistance mutations are more frequently generated in biofilms than in planktonic cells. These observations indicated that H. pylori biofilm formation may play an important role in preventing and controlling H. pylori infections. Therefore, investigation of H. pylori biofilm formation could be effective in elucidating the detailed mechanisms of infection and colonization by this microorganism.
The human gastric pathogen Helicobacter pylori forms biofilms in vitro and in vivo. The purpose of this study was to evaluate the effects of H. pylori biofilm formation in vitro on clarithromycin (CLR) susceptibility. CLR susceptibility of H. pylori intermediate (2-day) and mature (3-day) biofilms on glass coverslips was determined at concentrations from 0.03 to 0.5 µg/ml. H. pylori biofilm biomass was increased after treatment with CLR at minimum inhibitory concentration levels by up to 4-fold (2-day biofilm) and 16-fold (3-day biofilm). Minimum bactericidal concentrations of CLR against cells in a biofilm were higher (1.0 µg/ml) than that for planktonic cells (0.25 µg/ml). It was shown that the expression of efflux pump genes was significantly increased in biofilm cells. In addition, exposure of biofilms to CLR resulted in high level resistance generation compared to planktonic cells with increased resistance associated with the presence of a point mutation at either position 2142 or 2143 in the domain V loop of the 23S rRNA gene. These results demonstrate that H. pylori biofilm formation decreases the susceptibility to CLR and that H. pylori CLR resistance mutations are more frequently generated in biofilms than in planktonic cells.
Helicobacter pylori prevalence in Japanese children is approximately 1.8%, which is much lower than that reported in Japanese adults. New infection may be rare. Parent-to-child infection is thought to be the main infection route of the infrequent infection for children in Japan.
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