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Mol. Cells 2013; 35(2): 115-124

Published online February 21, 2013

https://doi.org/10.1007/s10059-013-2190-3

© The Korean Society for Molecular and Cellular Biology

Lipoteichoic Acid Isolated from Lactobacillus plantarum Suppresses LPS-Mediated Atherosclerotic Plaque Inflammation

Joo Yun Kim, Hangeun Kim, Bong Jun Jung, Na-Ra Kim, Jeong Euy Park, and Dae Kyun Chung

1Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin 449-701, Korea, 2Department of Internal Medicine, Saint Louis University, St. Louis, MO 63104, USA, 3Division of Cardiology, Samsung Medical Center and Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea, 4Skin Biotechnology Center, Kyung Hee University, Yongin 449-701, Korea, 5These authors contributed equally to this work.

Received: July 27, 2012; Revised: November 21, 2012; Accepted: November 21, 2012

Abstract

Chronic inflammation plays an important role in atherogenesis. Experimental studies have demonstrated the accumulation of monocytes/macrophages in athero-sclerotic plaques caused by inflammation. Here, we report the inhibitory effects of lipoteichoic acid (LTA) from Lactobacillus plantarum (pLTA) on atherosclerotic inflammation. pLTA inhibited the production of proinflammatory cytokines and nitric oxide in lipopolysaccharide (LPS)-stimu-lated cells and alleviated THP-1 cell adhesion to HUVEC by down-regulation of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-I), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. The inhibitory effect of pLTA was mediated by inhibition of NF-?B and activation of MAP kinases. Inhibition of monocyte/macrophage infil-tration to the arterial lumen was shown in pLTA-injected ApoE-/- mice, which was concurrent with inhibition of MMP-9 and preservation of CD31 production. The anti-inflammatory effect mediated by pLTA decreased expres-sion of atherosclerotic markers such as COX-2, Bax, and HSP27 and also cell surface receptors such as TLR4 and CCR7. Together, these results underscore the role of pLTA in suppressing atherosclerotic plaque inflammation and will help in identifying targets with therapeutic potential against pathogen-mediated atherogenesis.

Keywords ApoE, atherosclerosis, cytokine, Lactobacillus, lipoteichoic acid, inflammation

Article

Research Article

Mol. Cells 2013; 35(2): 115-124

Published online February 28, 2013 https://doi.org/10.1007/s10059-013-2190-3

Copyright © The Korean Society for Molecular and Cellular Biology.

Lipoteichoic Acid Isolated from Lactobacillus plantarum Suppresses LPS-Mediated Atherosclerotic Plaque Inflammation

Joo Yun Kim, Hangeun Kim, Bong Jun Jung, Na-Ra Kim, Jeong Euy Park, and Dae Kyun Chung

1Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin 449-701, Korea, 2Department of Internal Medicine, Saint Louis University, St. Louis, MO 63104, USA, 3Division of Cardiology, Samsung Medical Center and Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea, 4Skin Biotechnology Center, Kyung Hee University, Yongin 449-701, Korea, 5These authors contributed equally to this work.

Received: July 27, 2012; Revised: November 21, 2012; Accepted: November 21, 2012

Abstract

Chronic inflammation plays an important role in atherogenesis. Experimental studies have demonstrated the accumulation of monocytes/macrophages in athero-sclerotic plaques caused by inflammation. Here, we report the inhibitory effects of lipoteichoic acid (LTA) from Lactobacillus plantarum (pLTA) on atherosclerotic inflammation. pLTA inhibited the production of proinflammatory cytokines and nitric oxide in lipopolysaccharide (LPS)-stimu-lated cells and alleviated THP-1 cell adhesion to HUVEC by down-regulation of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-I), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. The inhibitory effect of pLTA was mediated by inhibition of NF-?B and activation of MAP kinases. Inhibition of monocyte/macrophage infil-tration to the arterial lumen was shown in pLTA-injected ApoE-/- mice, which was concurrent with inhibition of MMP-9 and preservation of CD31 production. The anti-inflammatory effect mediated by pLTA decreased expres-sion of atherosclerotic markers such as COX-2, Bax, and HSP27 and also cell surface receptors such as TLR4 and CCR7. Together, these results underscore the role of pLTA in suppressing atherosclerotic plaque inflammation and will help in identifying targets with therapeutic potential against pathogen-mediated atherogenesis.

Keywords: ApoE, atherosclerosis, cytokine, Lactobacillus, lipoteichoic acid, inflammation

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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