<i>Lactobacillus</i>plantarum inhibits epithelial barrier dysfunction and interleukin-8 secretion induced by tumor necrosis factor-α

Ko, Jae Sung

doi:10.3748/wjg.v13.i13.1962

Cited by 76 publications

(48 citation statements)

References 25 publications

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“…The results of this study provide a highly plausible explanation for the reported protective effects of L. plantarum and other probiotic strains on barrier disruption by inflammatory cytokines, chemicals, and infectious agents (13,18,20,28,32,34,35,48). However, increased mucin production, immunomodulation, pathogen inhibition, and effects on the resident microbiota could also be contributory factors, particularly in vivo.…”

Section: G855mentioning

confidence: 58%

“…In vitro studies using polarized Caco-2 cell monolayers have also shown protective effects of L. plantarum strains on the reduction of TER induced by tumor necrosis factor-␣ (TNF-␣) and Listeria monocytogenes (L. monocytogenes) (17,18). In the latter study, changes in the total amount of cellular ZO-1 were implicated in the opposing effects of L. plantarum and L. monocytogenes, but effects on TJ composition itself were not studied.…”

Section: Translational Highlights This Study Demonstrates That In Thmentioning

confidence: 99%

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Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Karczewski

Troost

Konings

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

543

390

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Karczewski J, Troost FJ, Konings I, Dekker J, Kleerebezem M, Brummer RM, Wells JM. Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier. Am J Physiol Gastrointest Liver Physiol 298: G851-G859, 2010. First published March 11, 2010; doi:10.1152/ajpgi.00327.2009.-Lactobacillus plantarum, a commensal bacterium of humans, has been proposed to enhance the intestinal barrier, which is compromised in a number of intestinal disorders. To study the effect of L. plantarum strain WCFS1 on human barrier function, healthy subjects were administered L. plantarum or placebo in the duodenum for 6 h by means of a feeding catheter. The scaffold protein zonula occludens (ZO)-1 and transmembrane protein occludin were found to be significantly increased in the vicinity of the tight-junction (TJ) structures, which form the paracellular seal between cells of the epithelium. In an in vitro model of the human epithelium, L. plantarum induced translocation of ZO-1 to the TJ region; however, the effects on occludin were minor compared with those seen in vivo. L. plantarum was shown to activate Toll-like receptor 2 (TLR2) signaling, and treatment of Caco-2 monolayers with the TLR2 agonist Pam 3 -Cys-SK4(PCSK) significantly increased fluorescent staining of occludin in the TJ. Pretreatment of Caco-2 monolayers with L. plantarum or PCSK significantly attenuated the effects of phorbol ester-induced dislocation of ZO-1 and occludin and the associated increase in epithelial permeability. Our results identifying commensal bacterial stimulation of TLR2 in the gut epithelium as a regulator of epithelial integrity have important implications for understanding probiotic mechanisms and the control of intestinal homeostasis. epithelium; intestine

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Section: G855mentioning

confidence: 58%

Section: Translational Highlights This Study Demonstrates That In Thmentioning

confidence: 99%

Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Karczewski

Troost

Konings

et al. 2010

American Journal of Physiology-Gastrointestinal and Liver Physi

543

390

View full text Add to dashboard Cite

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“…Exposure to pro-inflammatory cytokines IFN-c or TNF-a, individually, and over long time periods (36-48 h), decreases barrier function in model polarized epithelial monolayers (Ko et al, 2007;Ma et al, 2004;Utech et al, 2005). However, the two cytokines also act synergistically to impair epithelial barrier function (Wang et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus rhamnosus GG attenuates interferon-γ and tumour necrosis factor-α-induced barrier dysfunction and pro-inflammatory signalling

et al. 2010

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The intestinal epithelium forms a protective barrier against luminal contents and the external environment, mediated via intercellular tight junctions (TJs). The TJ can be disrupted via cell signalling induced by either enteric pathogens or pro-inflammatory cytokines, thereby contributing to various intestinal disorders ranging from acute infectious diarrhoea to chronic inflammatory bowel diseases. Probiotics, such as Lactobacillus rhamnosus GG (LGG), are reported to confer beneficial effects on epithelial cells, including antagonizing infections and reducing overt proinflammatory responses, but the underlying mechanisms of these observed effects require further characterization. We hypothesized that probiotics preserve barrier function by interfering with proinflammatory cytokine signalling. Caco-2bbe cells were seeded into Transwells to attain polarized monolayers with intercellular TJs. Monolayers were inoculated apically with the probiotic LGG 3 h prior to the addition of IFN-c (100 ng ml "1 ) to the basolateral medium overnight. The monolayers were then placed in fresh basal medium±TNF-a (10 ng ml "1) and transepithelial electrical resistance (TER) measurements were taken over the time-course of TNF-a stimulation. To complement the TER findings, cells were processed for zona occludens-1 (ZO-1) immunofluorescence staining. As a measure of TNF-a downstream signalling, cells were immunofluorescently stained for NF-kB p65 subunit and CXCL-8 mRNA was quantified by qRT-PCR. Basal cell culture medium was collected after overnight TNF-a stimulation to measure secreted chemokines, including CXCL-8 (interleukin-8) and . Following LGG inoculation, IFN-c priming and 24 h TNF-a stimulation, epithelial cells maintained TER and ZO-1 distribution.LGG diminished the nuclear translocation of p65, demonstrated by both immunofluorescence and CXCL-8 mRNA expression. CXCL-8 and CCL-11 protein levels were decreased in LGG-inoculated, cytokine-challenged cells. These findings indicate that LGG alleviates the effects of pro-inflammatory cytokines on epithelial barrier integrity and inflammation, mediated, at least in part, through inhibition of NF-kB signalling. INTRODUCTIONThe intestinal epithelium forms a protective barrier against luminal contents, such as microbes and dietary food antigens, present in the external environment. Barrier function is mediated through apical junction complexes, which consist of paracellular proteins integrated into tight junctions (TJs) (Van Itallie & Anderson, 2006). Abnormalities of intercellular TJs contribute to a variety of intestinal disorders, including acute diarrhoeal illness, gluten-sensitive enteropathy (coeliac disease) and chronic inflammatory bowel disease (McGuckin et al., 2009). The challenging of intact polarized epithelia with either proinflammatory cytokines or pathogenic bacteria dismantles the TJ protein structure and thereby disrupts barrier function (Donato et al., 2008; Wang et al., 2005Wang et al., , 2006 Zareie et al., 2005).We have shown that probiotic lactobacilli antago...

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“…Evidence has indicated that endogenous carbon monoxide (CO), a biproduct of inducible heme oxygenase can modulates inflammation. Many experiments have demonstrated that the administration of exogenous CO inhibits the lipopolysaccharide-induced production of cytokines both in vivo and in vitro, and consequently exhibits important cytoprotective functions and anti-inflammatory properties that are beneficial for the resolution of acute inflammation [16][17][18][19] . Recently, transitional metal carbonyls have been identified as potential CO-releasing molecules (CORM) with the potential to facilitate the pharmaceutical use of CO by delivering it to tissues and organs [20] .…”

Section: Introductionmentioning

confidence: 99%

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

Liu

Sun

et al. 2008

Acta Pharmacologica Sinica

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Aim: To determine whether carbon monoxide (CO)-releasing molecules-liberated CO suppress inflammatory cytokine production and oxidative stress in the small intestine of burnt mice. Methods: Twenty-eight mice were assigned to 4 groups. The mice in the sham group (n=7) underwent sham thermal injury, whereas the mice in the burn group (n=7) received 15% total body surface area full-thickness thermal injury, the mice in the burn+CO-releasing molecules (CORM)-2 group (n=7) underwent the same injury with immediate administration of CORM-2 (8 mg/kg, iv), and the mice in the burn+inactivated CORM (iCORM)-2 group (n=7) underwent the same injury with immediate administration of iCORM-2. The levels of inflammatory cytokines in the tissue homogenates were measured by ELISA. The levels of malondialdehyde (MDA), nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) in the small intestine were also assessed. In the in vitro experiment, Caco-2 cells were stimulated by experimental mouse sera (50%, v/v) for 4 h. Subsequently, the levels of interleukin (IL)-8 and NO in the supernatants were assessed. Reactive oxygen species (ROS) generation in Caco-2 cells was also measured. Results: The treatment of burnt mice with CORM-2 significantly attenuated the levels of IL-1β, TNF-α, MDA, and NO in tissue homogenates. This was accompanied by a decrease of iNOS expression. In parallel, the levels of IL-8, NO, and intracellular ROS generation in the supernatants of Caco-2 stimulated by the CORM-2-treated burnt mouse sera was markedly decreased. Conclusion: CORM-released CO attenuates the production of inflammatory cytokines, prevents burn-induced ROS generation, and suppresses the oxidative stress in the small intestine of burnt mice by interfering with the protein expression of iNOS.

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Lactobacillusplantarum inhibits epithelial barrier dysfunction and interleukin-8 secretion induced by tumor necrosis factor-α

Cited by 76 publications

References 25 publications

Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Lactobacillus rhamnosus GG attenuates interferon-γ and tumour necrosis factor-α-induced barrier dysfunction and pro-inflammatory signalling

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹

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Lactobacillusplantarum inhibits epithelial barrier dysfunction and interleukin-8 secretion induced by tumor necrosis factor-α

Cited by 76 publications

References 25 publications

Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Regulation of human epithelial tight junction proteins by Lactobacillus plantarum in vivo and protective effects on the epithelial barrier

Lactobacillus rhamnosus GG attenuates interferon-γ and tumour necrosis factor-α-induced barrier dysfunction and pro-inflammatory signalling

Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice1

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Suppression of inflammatory cytokine production and oxidative stress by CO-releasing moleculesliberated CO in the small intestine of thermally-injured mice¹