Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation
A biofilm is an aggregate of microorganisms in which cells adhere to biological or non-biological surfaces and is responsible for various infectious diseases. Infections caused by Staphylococcus aureus, including pneumonia, endocarditis, and osteomyelitis, are often associated with colonization and...
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doaj-ed5e643063f24bb99ad0e7ca32e33a462020-11-25T01:05:09ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2018-02-01910.3389/fmicb.2018.00327323594Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm FormationKi Bum Ahn0Ki Bum Ahn1Jung Eun Baik2Cheol-Heui Yun3Seung Hyun Han4Department of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul, South KoreaResearch Division for Biotechnology, Korea Atomic Energy Research Institute, Jeongeup, South KoreaDepartment of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul, South KoreaDepartment of Agricultural Biotechnology and Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, South KoreaDepartment of Oral Microbiology and Immunology, DRI, and BK21 Plus Program, School of Dentistry, Seoul National University, Seoul, South KoreaA biofilm is an aggregate of microorganisms in which cells adhere to biological or non-biological surfaces and is responsible for various infectious diseases. Infections caused by Staphylococcus aureus, including pneumonia, endocarditis, and osteomyelitis, are often associated with colonization and biofilm formation. Although lipoteichoic acid (LTA) is involved in biofilm formation, the specific role of LTA is not clearly understood. In this study, we demonstrated that LTA released from Lactobacillus plantarum could inhibit S. aureus biofilm formation and aggregation without affecting the growth of S. aureus in various in vitro and in vivo models. L. plantarum LTA (Lp.LTA) also inhibited biofilm formation of S. aureus clinical isolates, including a methicillin-resistant strain. Remarkably, Lp.LTA not only interfered with S. aureus biofilm formation, but it also disrupted a pre-formed biofilm. Mechanism studies demonstrated that Lp.LTA inhibited expression of the ica-operon, which is responsible for the production of poly-N-acetylglucosamine, a key molecule required for S. aureus biofilm development. Lp.LTA increased the release of autoinducer-2 from S. aureus, which contributed to the inhibition of S. aureus biofilm formation. Moreover, Lp.LTA treatment enhanced susceptibility of the biofilm to various antibiotics and to macrophages. Interestingly, Lp.LTA without D-alanine moieties was not able to inhibit biofilm formation by S. aureus. In conclusion, the present study suggests that LTA can inhibit S. aureus biofilm formation, and therefore could be applied for preventing and/or treating infectious diseases caused by S. aureus biofilms.http://journal.frontiersin.org/article/10.3389/fmicb.2018.00327/fulllipoteichoic acidLactobacillus plantarumStaphylococcus aureusbiofilm formationinfectious diseases |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ki Bum Ahn Ki Bum Ahn Jung Eun Baik Cheol-Heui Yun Seung Hyun Han |
spellingShingle |
Ki Bum Ahn Ki Bum Ahn Jung Eun Baik Cheol-Heui Yun Seung Hyun Han Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation Frontiers in Microbiology lipoteichoic acid Lactobacillus plantarum Staphylococcus aureus biofilm formation infectious diseases |
author_facet |
Ki Bum Ahn Ki Bum Ahn Jung Eun Baik Cheol-Heui Yun Seung Hyun Han |
author_sort |
Ki Bum Ahn |
title |
Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation |
title_short |
Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation |
title_full |
Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation |
title_fullStr |
Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation |
title_full_unstemmed |
Lipoteichoic Acid Inhibits Staphylococcus aureus Biofilm Formation |
title_sort |
lipoteichoic acid inhibits staphylococcus aureus biofilm formation |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Microbiology |
issn |
1664-302X |
publishDate |
2018-02-01 |
description |
A biofilm is an aggregate of microorganisms in which cells adhere to biological or non-biological surfaces and is responsible for various infectious diseases. Infections caused by Staphylococcus aureus, including pneumonia, endocarditis, and osteomyelitis, are often associated with colonization and biofilm formation. Although lipoteichoic acid (LTA) is involved in biofilm formation, the specific role of LTA is not clearly understood. In this study, we demonstrated that LTA released from Lactobacillus plantarum could inhibit S. aureus biofilm formation and aggregation without affecting the growth of S. aureus in various in vitro and in vivo models. L. plantarum LTA (Lp.LTA) also inhibited biofilm formation of S. aureus clinical isolates, including a methicillin-resistant strain. Remarkably, Lp.LTA not only interfered with S. aureus biofilm formation, but it also disrupted a pre-formed biofilm. Mechanism studies demonstrated that Lp.LTA inhibited expression of the ica-operon, which is responsible for the production of poly-N-acetylglucosamine, a key molecule required for S. aureus biofilm development. Lp.LTA increased the release of autoinducer-2 from S. aureus, which contributed to the inhibition of S. aureus biofilm formation. Moreover, Lp.LTA treatment enhanced susceptibility of the biofilm to various antibiotics and to macrophages. Interestingly, Lp.LTA without D-alanine moieties was not able to inhibit biofilm formation by S. aureus. In conclusion, the present study suggests that LTA can inhibit S. aureus biofilm formation, and therefore could be applied for preventing and/or treating infectious diseases caused by S. aureus biofilms. |
topic |
lipoteichoic acid Lactobacillus plantarum Staphylococcus aureus biofilm formation infectious diseases |
url |
http://journal.frontiersin.org/article/10.3389/fmicb.2018.00327/full |
work_keys_str_mv |
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