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.
- SourceAvailable from: Victoria Davenport[Show abstract] [Hide abstract]
ABSTRACT: In this study, we investigate the potential for oral Lactobacilli (LB) to afford innate protection against nasopha- ryngeal coloniser Neisseria meningitidis serogroup B (NmB), which causes the bulk of UK meningococcal disease. Oral isolates of L. plantarum, L. salivarious, L. casei, L. rhamnosus, L. gasseri and gut probiotic L. rhamnosus GG were assessed for their ability to suppress nasopharyngeal epithelial inflammatory responses to pathogenic NmB. The specificity of attenuation was examined using TLR 2 ligand, Pam3Cys, and early response cytokine IL1β; and the mechanism of attenuation was explored using heat-killed organisms and conditioned medium. Pro-in- flammatory IL-6 and TNFα cytokine secretion was quantified by ELISA and associated cell death was quantified by PI staining and LDH release. NmB adhesion, invasion and metabolism were determined using standard gen- tamicin protection with viable counts, and bioluminescence, respectively. L. plantarum and L. salivarious sup- pressed IL-6 and TNFα secretions from NmB-infected epithelial cells. LB did not need to be alive and could sup- press using secretions, which were independent of TLR2 or IL1β receptor signalling. L. plantarum, in particular, reduced NmB-induced necrotic cell death of epithelial monolayers. Like L. salivarious, it significantly inhibited NmB adhesion but uniquely L. plantarum abolished NmB invasion. Using bioluminescence as a reporter of pa- thogen metabolism, L. plantarum and its secretions were found to inhibit NmB metabolism during cell invasion assays. We conclude that oral L. plantarum and its secretions could be used to help reduce the burden of menin- gococcal disease by removing the intracellular nasopharyngeal reservoir of NmB.Advances in microbiology. 01/2014; 4:81-93.
Article: Gut ecosystem: how microbes help us.[Show abstract] [Hide abstract]
ABSTRACT: The human gut houses one of the most complex and abundant ecosystems composed of up to 1013-1014 microorganisms. Although the anthropocentric concept of life has concealed the function of microorganisms inside us, the important role of gut bacterial community in human health is well recognised today. Moreover, different microorganims, which are commonly present in a large diversity of food products, transit through our gut every day adding in some cases a beneficial effect to our health (probiotics). This crosstalk is concentrated mainly in the intestinal epithelium, where microbes provide the host with essential nutrients and modulation of the immune system. Furthermore, microorganisms also display antimicrobial activities maintaining a gut ecosystem stable. This review summarises some of the recent findings on the interaction of both commensal and probiotic bacteria with each other and with the host. The aim is to highlight the cooperative status found in healthy individuals as well as the importance of this crosstalk in the maintenance of human homeostasis.Beneficial Microbes 02/2014; · 1.47 Impact Factor
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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. · 2.98 Impact Factor