Lactobacillus plantarum lipoteichoic acid down-regulated Shigella flexneri peptidoglycan-induced inflammation
ABSTRACT Bacterial peptidoglycans (PGNs) are recognized by the host's innate immune system. This process is mediated by the NOD/CARD family of proteins, which induces inflammation by activating nuclear factor (NF)-κB. Excessive activation of monocytes by Shigella flexneri PGN (flexPGN) leads to serious inflammatory diseases such as intestinal bowel diseases (IBD) and Crohn's disease. In this study, we examined whether Lactobacillus plantarum lipoteichoic acid (pLTA) could attenuate the pro-inflammatory signaling induced by flexPGN in human monocytic THP-1 cells. Compared to control THP-1 cells, pLTA-tolerant cells showed a significant reduction in TNF-α and IL-1β production in response to flexPGN. We also examined the inhibition of NF-κB and the activation of mitogen-activated protein kinase (MAPK) in pLTA-tolerant cells. We found that the expression of NOD2 in pLTA-tolerant cells was down-regulated at the mRNA and protein levels, suggesting that pLTA is a potent modulator of the pro-inflammatory NOD2-related signaling pathways induced by flexPGN. Together, these data indicate that pLTA induces cross-tolerance against flexPGN. Notably, these effects are related not only to IL-1 signaling, which is known to play a role in LPS tolerance, but also to NOD-Rick signaling. This study provides insight into how commensal microflora may contribute to homeostasis of the host intestinal tract.
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- "It is also one of the dominant Lactobacillus species in the hosts’ intestinal tract. Recent studies have shown that some strains of Lactobacillus plantarum attenuate inflammation induced by Shigella flexneri peptidoglycan by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), inactivating mitogen-activated protein kinase (MAPK), and reducing NOD2 mRNA expression as well as protein levels, the actions which in turn lead to a decrease in pro-inflammatory cytokine secretion . Moreover, van Baarlen et al. [17,18] demonstrated that even dead L. plantarum can exert beneficial functions protecting the host against the enormous array of commensal bacteria in the gut via epithelial crosstalk of mucosal interface microbiota. "
ABSTRACT: Crohn's disease and ulcerative colitis are the major types of chronic inflammatory bowel disease occurring in the colon and small intestine. A growing body of research has proposed that probiotics are able to attenuate the inflammatory symptoms of these diseases in vitro and in vivo. However, the mechanism of probiotic actions remains unclear. Our results suggested Lactobacillus plantarum MYL26 inhibited inflammation in Caco-2 cells through regulation of gene expressions of TOLLIP, SOCS1, SOCS3, and IkappaBalpha, rather than SHIP-1 and IRAK-3. We proposed that live/ heat-killed Lactobacillus plantarum MYL26 and bacterial cell wall extract treatments impaired TLR4-NFkappab signal transduction through Tollip, SOCS-1 and SOCS-3 activation, thus inducing LPS tolerance. Our findings suggest that either heat-killed probiotics or probiotic cell wall extracts are able to attenuate inflammation through pathways similar to that of live bacteria.BMC Microbiology 08/2013; 13(1):190. DOI:10.1186/1471-2180-13-190 · 2.73 Impact Factor
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- "Finally, a study carried out on human monocytic THP-1 cells has revealed that LTAs purified from L. plantarum K8 (KCTC10887BP) are potent modulators of the proinflammatory NOD2-related signalling pathway triggered by the PGN of Shigella flexneri KCTC 2517, as demonstrated by downregulation of NOD2 expression at the mRNA and protein levels. In this study, LTAs purified from the L. plantarum K8 strain induced cross-tolerance and inhibited excessive inflammatory responses induced by the pathogenic components (Kim et al. 2011). At the end of this short discussion on the immunomodulatory properties attributed to cell wall constitutive macromolecules, it appears however of importance mentioning that the contamination of cell wall preparations by other cell envelope components can be hardly avoided and monitored. "
ABSTRACT: The probiotic approach represents a potentially effective and mild alternative strategy for the prevention and treatment of either inflammatory or allergic diseases. Several studies have shown that different bacterial strains can exert their probiotic abilities by influencing the host's immune system, thereby modulating immune responses. However, the emerging concern regarding safety problems arising from the extensive use of live microbial cells is enhancing the interest in non-viable microorganisms or microbial cell extracts, as they could eliminate shelf-life problems and reduce the risks of microbial translocation and infection. The purpose of this review is to provide an overview of the scientific literature concerning studies in which dead microbial cells or crude microbial cell fractions have been used as health-promoting agents. Particular attention will be given to the modulation of host immune responses. Possible mechanisms determining the effect on the immune system will also be discussed. Finally, in the light of the FAO/WHO definition of probiotics, indicating that the word 'probiotic' should be restricted to products that contain live microorganisms, and considering the scientific evidence indicating that inactivated microbes can positively affect human health, we propose the new term 'paraprobiotic' to indicate the use of inactivated microbial cells or cell fractions to confer a health benefit to the consumer.Genes & Nutrition 04/2011; 6(3):261-74. DOI:10.1007/s12263-011-0218-x · 2.79 Impact Factor
Conference Paper: Transmyocardial revascularization with Ho:YAG lasers[Show abstract] [Hide abstract]
ABSTRACT: A Ho:YAG laser used for transmyocardial revascularization can produce histology similar to a CO<sub>2</sub> laser, potentially permitting the procedure to be done with less invasive fiber-optic delivery systems. Thoracoscopic and percutaneous systems are under developmentLasers and Electro-Optics Society Annual Meeting, 1995. 8th Annual Meeting Conference Proceedings, Volume 1., IEEE; 11/1995