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

Abstract

Chronic inflammation plays an important role in atherogenesis. Experimental studies have demonstrated the accumulation of monocytes/macrophages in atherosclerotic 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)-stimulated 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-κB and activation of MAP kinases. Inhibition of monocyte/macrophage infiltration to the arterial lumen was shown in pLTAinjected ApoE -/-mice, which was concurrent with inhibition of MMP-9 and preservation of CD31 production. The antiinflammatory effect mediated by pLTA decreased expression 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.

Retracted: Interleukin‐1 blockade treatment decreasing cardiovascular risk

“…The process of inflammation mediated by IL-1 can cause many kinds of diseases. [5][6][7] Long-term chronic inflammation can lead to the formation of arterial plaques as well as atherogenesis, 8 and active inflammatory process may trigger the rupture of plaque which increasing the risk of coronary thrombosis, then leading to clinical ischemic events. 9 There are four IL-1 blockers available now, anakinra, canakinumab, rilonacept, and gevokizumab.…”

The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques

“…The deposition of the lipids and oxLDL causes activation of innate and adaptive immunity leading to increased production of inflammatory cytokines and homing of inflammatory cells. Infection of the arterial intima with viruses and bacteria results in the production of pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharides (LPS), peptidoglycans, and lipoteichoic acid (Chen et al 2013;Kim et al 2013;Thankam et al 2016) (Figures 2 and 3). Here, we have discussed the role of DAMPs and PAMPs and their interaction with inflammatory mediators in the pathogenesis of inflammation-mediated plaque vulnerability.…”

Molecules Produced by Probiotics and Intestinal Microorganisms with Immunomodulatory Activity

“…The results indicated that LTA of L. plantarum can modulate pro-inflammatory or anti-inflammatory responses. Subsequent studies showed other immunomodulatory features of L. plantarum LTA, such as the down-regulation of Shigella flexneri peptidoglycan-induced inflammation [43], or the suppression of LPS-mediated inflammation [44], among other effects. LTA function has also been studied in L. rhamnosus GG (LGG), one of the most studied probiotics [45].…”