Antioxidants counteract lipopolysaccharide-triggered alterations of human colonic smooth muscle cells

Matarrese, Paola; Petitta, C.; Scirocco, Annunziata; Ascione, Barbara; Ammoscato, Francesca; Natale, Giuseppe Di; Anastasi, Emanuela; Marconi, Matteo; Chirletti, Piero; Malorni, Walter; Severi, Carola

doi:10.1016/j.freeradbiomed.2012.09.022

Cited by 16 publications

(26 citation statements)

References 44 publications

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“…Conversely, high fiber diets are expected to reduce LPS exposures via alteration of microbial composition, improvement in the mucosal barrier function through facilitating tight junction assembly and reduction in epithelial permeability through production of short chain fatty acids (133–136). Likewise, dietary antioxidants can counteract the adverse effects of LPS exposure in colon smooth muscle cells (137). …”

Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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Obesity increases the risks of many cancers. One important mechanism behind this association is the obesity-associated pro-inflammatory state. Although the composition of the intestinal microbiome undoubtedly can contribute to the pro-inflammatory state, perhaps the most important aspect of host-microbiome interactions is host exposure to components of intestinal bacteria that stimulate the inflammatory reactions. Systemic exposures to intestinal bacteria can be modulated by dietary factors by altering both the composition of the intestinal microbiota as well as absorption of bacterial products from the intestinal lumen. In particular, high fat and high energy diets have been shown to facilitate absorption of bacterial lipopolysaccharide (LPS) from intestinal bacteria. Biomarkers of bacterial exposures that have been measured in blood include LPS-binding protein, sCD14, fatty acids characteristic of intestinal bacteria and immunoglobulins specific for bacterial LPS and flagellin. The optimal strategies to reduce these pro-inflammatory exposures, whether by altering diet composition, avoiding a positive energy balance or reducing adipose stores, likely differ in each individual. Biomarkers that assess systemic bacterial exposures therefore should be useful to optimize and personalize preventive approaches for individuals and groups with specific characteristics, and to gain insight into the possible mechanisms involved with different preventive approaches.

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Section: Diet Modulates Absorption Of Bacterial Componentsmentioning

confidence: 99%

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Djurić

2017

Translational Research

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“…Prolonged activation of this pathway produces a persistent inflammatory cytopathic oxidative imbalance and consequent NF‐κB activation that leads to the de‐differentiation of SMC toward the so‐called synthetic phenotype. This phenotype persists after LPS‐washout and contributes to muscle dysfunction . As Lactobacillus paracasei has been shown to normalize smooth muscle hyper‐contractility in a murine postinfective irritable bowel syndrome model, it can be hypothesized that these protective effects of Lactobacillus could occur, as in cardiomyocytes, also in enteric muscle.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus rhamnosus protects human colonic muscle from pathogen lipopolysaccharide‐induced damage

Ammoscato

Scirocco

Altomare

et al. 2013

Neurogastroenterology Motil

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Key Messages• Lactobacillus rhamnosus (LGG) interferes with inflammatory reaction triggered by infection in human colonic muscle. Therefore, this study provides a rational design for clinical studies in which the efficacy of probiotics in bacterial-related gut motor disorders could ultimately be determined.• Aim of the study was to investigate the possible protective effects of LGG, and of its derived products (culture supernatant), on LPS-induced morphofunctional alterations of human colonic smooth muscle.• Surgical specimen of human colon were used to obtained muscle strips and isolated cells. Experimental samples were exposed either to the sole LGG or to LPS, in the presence or absence of the probiotic or its supernatant.• LGG, as well as its culture supernatant, activate an intrinsic myogenic response able to counteract LPS proinflammatory burst and to protect human gastrointestinal smooth muscle from LPS-induced damage. These effects occur via a direct involvement of TLR2 expressed on human colonic smooth muscle cells. AbstractBackground Lactobacillus species might positively affect gastrointestinal motility. These Gram-positive bacteria bind Toll-like receptor 2 (TLR2) that elicits anti-inflammatory activity and exerts protective effects on damage induced by lipopolysaccharide (LPS). Whether such effect occurs in gastrointestinal smooth muscle has not been established yet. Aim of this study was to characterize the effects of Lactobacillus rhamnosus GG (LGG) and of supernatants harvested from LGG cultures on human colonic smooth muscle and to explore their protective activity against LPS-induced myogenic morpho-functional alterations. Methods The effects of LGG (ATCC 53103 strain) and of supernatants have been tested on both human colonic smooth muscle strips and isolated cells in the absence or presence of LPS obtained from a pathogenic strain of Escherichia coli. Their effects on myogenic morpho-functional properties, on LPS-induced NFjB activation, and on cytokine production have been evaluated. Toll-like receptor 2 expression has been analyzed by qPCR and flow cytometry. Key Results Lactobacillus rhamnosus GG exerted negligible transient effects per se whereas it was capable of activating an intrinsic myogenic response counteracting LPS-induced alterations. In particular, both LGG and supernatants significantly reduced the LPS-induced morpho-functional alterations of muscle cells, i.e. cell shortening and inhibition of contractile response. They also hindered LPS-induced pro-inflammatory effects by decreasing Address for Correspondence

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“…Although the exact mechanisms whereby LPS is able to impair muscle contractility are still to be established, various targets have been demonstrated. LPS can directly activate muscular TLR4 inducing a time- and concentration-dependent impairment of contractility associated to cytoskeleton alterations, together with an intracellular oxidative imbalance as shown on human colonic smooth muscle cells[79] (Figure 2). Many of these effects persisted even after LPS withdrawn suggesting that motility dysfunction might play a pivotal role both during an acute infective process and after its resolution.…”

Section: Direct Effectsmentioning

confidence: 99%

Gastrointestinal neuromuscular apparatus: An underestimated target of gut microbiota

Guarino¹,

Cicala²,

Putignani³

et al. 2016

WJG

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Over the last few years, the importance of the resident intestinal microbiota in the pathogenesis of several gastro-intestinal diseases has been largely investigated. Growing evidence suggest that microbiota can influence gastro-intestinal motility. The current working hypothesis is that dysbiosis-driven mucosal alterations induce the production of several inflammatory/immune mediators which affect gut neuro-muscular functions. Besides these indirect mucosal-mediated effects, the present review highlights that recent evidence suggests that microbiota can directly affect enteric nerves and smooth muscle cells functions through its metabolic products or bacterial molecular components translocated from the intestinal lumen. Toll-like receptors, the bacterial recognition receptors, are expressed both on enteric nerves and smooth muscle and are emerging as potential mediators between microbiota and the enteric neuromuscular apparatus. Furthermore, the ongoing studies on probiotics support the hypothesis that the neuromuscular apparatus may represent a target of intervention, thus opening new physiopathological and therapeutic scenarios.

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Antioxidants counteract lipopolysaccharide-triggered alterations of human colonic smooth muscle cells

Cited by 16 publications

References 44 publications

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Obesity-associated cancer risk: the role of intestinal microbiota in the etiology of the host proinflammatory state

Lactobacillus rhamnosus protects human colonic muscle from pathogen lipopolysaccharide‐induced damage

Gastrointestinal neuromuscular apparatus: An underestimated target of gut microbiota

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